There’s a Hole in My Head 

I’m in the middle of having a root canal. The last time I had one was just about the time I was diagnosed with chronic kidney disease, a little more than 13 years ago. Since then, I’ve written about periodontal issues, dry mouth, Novocain, but not about the connection between diabetes, ckd, and dental issues. That’s what I’ll be dealing with today. 

Let’s start at the very beginning with an explanation of root canal. The American Association of Endodontists [Endodontists treat the soft tissue inside your teeth.] had an easily understood explanation: 

“Endodontic treatment can often be performed in one or two visits and involves the following steps: 

The endodontist examines and takes a radiograph of the tooth using x-rays, then administers local anesthetic. After the tooth is numb, the endodontist places a small protective sheet called a ‘dental dam’ over the area to isolate the tooth and keep it clean and free of saliva during the procedure. 

The endodontist makes an opening in the crown of the tooth. Very small instruments are used to clean the pulp from the pulp chamber and root canals and to shape the space for filling. 

After space is cleaned and shaped, the endodontist fills the root canals with a biocompatible material, usually a rubber-like material called gutta-percha. The gutta-percha is placed with an adhesive cement to ensure complete sealing of the root canals. In most cases, a temporary filling is placed to close the opening. The temporary filling will be removed by your dentist before the tooth is restored. 

After the final visit with your endodontist, you must return to your dentist to have a crown or other restoration placed on the tooth to protect and restore it to full function.” 

Photo by Evelina Zhu on Pexels.com

Got it? By the way, it really doesn’t hurt and there’s just a bit of an ache for the first day or so due to the pressure that had been exerted. At least, that’s the way it was for me. 

Now let’s see what we can find out about the kidney connection with a root canal. DaVita, a dialysis center which also educates about CKD, had just what I was looking for: 

 “Both tooth decay and gum disease can lead to infections that can cause problems for people with kidney disease and those who have diabetes…. 

Tooth decay and gum disease are caused by plaque. Plaque is a sticky film of bacteria that coats the teeth. The sugars and starches of the food you eat react with the plaque, causing it to release acids. These acids wear away the hard tooth enamel, eventually leading to cavities and tooth decay…. 

Gum disease starts when plaque accumulates and hardens over time. This hardened plaque is called tartar. Tartar settles at your gum line and can make your gums sensitive and irritated. If you notice your gums bleed after brushing your teeth, this is a symptom of gingivitis, an early stage of gum disease. Left untreated, tartar can build up to the point where the gums pull away from your teeth. This gap forms pockets that let in food and bacteria, which can cause infections. This stage of gum disease is called periodontitis…. 

A study in the Journal of Clinical Periodontology reported that people with kidney disease and those on dialysis are more likely to have periodontal disease and other oral health problems than the general population. Buildup of bacteria in the mouth can cause infection. Because people with kidney disease have weakened immune systems, they are more susceptible to infections…. 

Kidney patients are advised to tell their kidney doctor when a dental procedure is required. The doctor may recommend antibiotics be taken prior to the procedure to help guard against infection. [My endodontist prescribed them after my first treatment with him.] The dentist should be made aware that their patient has kidney disease or is on dialysis. [I told him before we started treatment that I have ckd.] Ideally, dental procedures, such as tooth extraction, should occur on a non-dialysis day for those on hemodialysis. Heparin, administered during hemodialysis, may cause some people to have extra bleeding.” 

I wanted to know how the pulp got infected in the first place. [That’s me: always asking “Why?”] I also wanted to be able to understand the answer. WebMD filled the bill: 

“A tooth’s pulp can become irritated, inflamed, and infected due to deep decay, repeated dental procedures on a tooth, large fillings, a crack or chip in the tooth, or trauma to the face.” 

Photo by Alex Green on Pexels.com

In my case, it was the large filling who knows how many years ago. So there I was with ckd, diabetes, and needing a root canal.  I knew my immune system wasn’t great and so did the endodontist; hence, the antibiotics. What I didn’t know was that dental problems could trigger other infections for those with ckd or diabetes. What I didn’t know was that this minor infection could become a major one because my immune system was weak due to the ckd and diabetes. 

Let me remind you why our immune systems are weak. I included this in SlowItDownCKD 2020

“So, what’s this immune system I mentioned? I turned to Medline Plus, a part of the U.S. National Library of Medicine which, in turn, is a division of the National Institutes of Health ‘Your immune system is a complex network of cells, tissues, and organs that work together to defend against germs. It helps your body to recognize these ‘foreign’ invaders. Then its job is to keep them out, or if it can’t, to find and destroy them’“  

It made more sense when I added this in the same blog, 

“According to the National Kidney Foundation, 

‘…Having kidney disease and kidney failure can weaken your immune system, making it easier for infections to take hold.  In fact, doctors and researchers have found that most infections, …, are worse in people with kidney disease.  People with a kidney transplant also have weakened immune systems.  This is because antirejection medicines (‘immunosuppressants’), which protect the body from rejecting the transplanted kidney, suppress the immune system’.” 

There you have it – the connection between CKD, diabetes, and a root canal. 

Until next week, 

Keep living your life! 

Water, Water, Everywhere

 As Chronic Kidney Disease patients, we are warned that we need to keep hydrating. That seems to be the current term for adequate water intake. I just call it drinking water. Surprise! Drinking too much water can also be harmful to your kidneys. 

I know; this is a shock. Let’s go back to the beginning to see why you need water for your health in the first place. Of course, the National Kidney Foundation came to mind immediately, and with good reason. They are a trusted source. This is their explanation. 

Photo by Pixabay on Pexels.com

“Keep your kidneys healthy by being ‘water wise.’ This means drinking the right amount of water for you. A common misconception is that everyone should drink eight glasses of water per day, but since everyone is different, daily water needs will vary by person. How much water you need is based on differences in age, climate, exercise intensity, as well as states of pregnancy, breastfeeding, and illness. 

About 60-70% of your body weight is made up of water, and every part of your body needs it to function properly. Water helps the kidneys remove wastes from your blood in the form of urine. Water also helps keep your blood vessels open so that blood can travel freely to your kidneys, and deliver essential nutrients to them. But if you become dehydrated, then it is more difficult for this delivery system to work. Mild dehydration can make you feel tired, and can impair normal bodily functions. Severe dehydration can lead to kidney damage, so it is important to drink enough when you work or exercise very hard, and especially in warm and humid weather.” 

That sounds reasonable, so what is this about too much water? Last February, PubMed published a study about this. By the way, PubMed is part of the National Center for Biotechnology [NCBI] which, in turn, is part of the National Library of Medicine [NLM]. That, in turn, is part of the National Institutes of Health [NIH]. This is what that study concluded. 

“In patients with CKD, the relation between plain water intake and progression to kidney failure appears to be U-shaped. Both low and high intake may not be beneficial in CKD.” 

Wait a minute here. Maybe we’d better find out more specifically how it is that water benefits the kidneys. Medical News Today had the answers I was looking for. 

“Water helps dissolve minerals and nutrients, making them more accessible to the body. It also helps remove waste products. 

The kidneys play a key role in balancing fluid levels. 

These two functions make water vital to the kidneys. 

Every day, the kidneys filter around 120-150 quarts of fluid. 

Of these, approximately 1-2 quarts are removed from the body in the form of urine, and the rest is recovered by the bloodstream. 

Water is essential for the kidneys to function. 

If the kidneys do not function properly, waste products and excess fluid can build up inside the body. 

Untreated, chronic kidney disease can lead to kidney failure. The organs stop working, and either dialysis or kidney transplantation is required.” 

It’s clear that water intake is essential for keeping our kidneys as healthy as possible, even though we have CKD. So, how can you cause damage by drinking too much water? The Mayo Clinic tells us: 

“Drinking too much water is rarely a problem for healthy, well-nourished adults. Athletes occasionally may drink too much water in an attempt to prevent dehydration during long or intense exercise. When you drink too much water, your kidneys can’t get rid of the excess water. The sodium content of your blood becomes diluted. This is called hyponatremia and it can be life-threatening.” 

I wanted a bit more about hyponatremia. I knew that hypo means ‘low’ from that Greek and Latin Roots one credit course I took to fill out my course requirements in undergraduate school. It turned out to be one of the more enjoyable courses I took. Anyway, back to hyponatremia.’Natr’ means sodium in medical terms and ’emia’ is the Greek suffix for blood. Add them together and you get low sodium in the blood. Notice, it’s not that you’re adding sodium, but rather that you’re diluting the existing sodium. 

So far, we’ve figured out we can’t drink too little or too much water if we want to keep whatever kidney function we have left. Does that mean we need to drink exactly eight glasses of water a day just as common knowledge tells us to? That’s not what we readdiscovered earlier in the blog. Welll, how does water balance in our bodies work then?

Funny you should ask. I was just reading an article by Tamara Hew-Butler, associate professor of exercise and sports science at Wayne State University, about this. She says,

“Because total body water balance, or what we exercise scientists call homeostasis, is complicated, mammals survive by making real-time adjustments at the kidney. That’s why when it comes to hydration, our kidneys are king. 

Within each kidney — we need only one (we are born with a spare, just in case) — is an undercover network of aquaporin-2 (AQP-2) water channels which respond to a hormone called arginine vasopressin. This is the body’s main anti-diuretic (water retention) hormone. It is secreted by the posterior pituitary gland in response to nerve signals sent from specialized brain sensors which detect subtle changes in water balance. These specialized sensors are called circumventricular organs. 

The kidneys will make molecular adjustments to both underhydration and overhydration within 40 seconds in response to any upset in the water balance. These adjustments result from the mobilization armies of AQP-2 water channels, numbering about 12 million per collecting duct cell. 

This is why when we drink more water than our body needs — above thirst — we immediately have to discharge any excess water. Or when we forget our water bottle during practice, we stop urinating to conserve body water. This quick coordinated action between the brain, cranial nerves and kidneys is far more efficient and precise than any phone app, gadget or personalized recommendation available.” 

I have to admit the scientific information about overhydrating is new to me. I find it fascinating and could go on and on about it, but it will take several blogs to do so. 

Until next week, 

Keep living your life! 

Podocytes Revisited

I haven’t written about these important little guys in almost a decade, so I thought it might be time. Way back then, I introduced them in SlowItDownCKD 2011.  

“Hope for Treating Chronic Kidney Disease Via Regeneration of Specialized Cells 

                 by Kathy Jones on December 06, 2011, at 7:26 PM                     Genetics & Stem Cells News         

Pedocytes are specialized type of epithelial cells in the kidney, which get damaged in more than 90 percent of all chronic kidney disease cases. 

 Now researchers at the Stanford University School of Medicine have uncovered an unexpected pathway that reveals for the first time how these cells may regenerate and renew themselves during normal kidney function. 

This finding is an important step toward one day therapeutically coaxing the cells to divide, which could be used to treat people with chronic kidney disease. 

‘Researchers have studied these cells for years, but the prevailing view has been that they don’t renew themselves,’ said associate professor of medicine Steven Artandi, MD, PhD. ‘Now we’ve found that podocytes can enter and leave the cell cycle in response to certain common signaling pathways.’ …. 

Podocytes are found only in the kidney and are an integral structural component of its blood-filtering system. They stand shoulder-to-shoulder in a part of the organ called the glomerulus and wrap their long ‘feet’ [Gail here: ped means foot in Latin, while pod means foot in Greek] the semi-permeable capillaries through which blood flows. Narrow slits between the feet allow small molecules, such as water and salts, to pass while blocking large proteins. 

This filtering process is the first step to forming urine, and it is critically important — even one missing cell can leave a gap that would allow unwanted molecules through the barrier. (Imagine wrapping your hands around a length of leaky garden hose so that the water seeps out between your fingers. Lift up one finger and you’re liable to get sprayed in the face.) 

This may be why previous researchers searching for signs of self-renewal in podocytes were unsuccessful, because any such renewal or replacement would likely need to be carefully orchestrated to avoid compromising the filtration system. As a result, scientists have been forced to conclude that the podocytes rarely, if ever, divided. 

‘It used to be thought that you were born with podocytes, and you died with the same podocytes — you don’t make any more during your lifetime,’ said Artandi. The only exception was certain rare types of kidney disease in which the podocytes abandon their blood-filtration duties en masse to de-differentiate into less-specialized, dividing cells that little resemble their predecessors. As a result, the glomerulus collapses and the patients’ kidneys begin to fail. One such disease is HIV-associated nephropathy, or HIVAN. 

The problem was, such a scenario doesn’t make a lot of evolutionary sense — particularly when other epithelial cells routinely regenerate themselves. ‘Podocytes are vitally important, and are also under enormous physical stress,’ said Artandi. ‘It’s hard to understand why we would have such a vulnerable blood-filtration system.’ 

To understand more about kidney biology, Artandi and Shkreli investigated the role of a protein component of the telomerase complex called TERT. Although telomerase is best known as an enzyme involved in cell aging, recent research in Artandi’s lab and others have shown that TERT also plays a role in many types of cellular regeneration. 

The researchers found that temporarily increasing the expression of TERT in adult, otherwise healthy laboratory mice caused the formerly stolid podocytes to abruptly de-differentiate and begin dividing. As a result, the glomerulus collapsed in a way that resembles what happens in humans with HIVAN. Conversely, ceasing the overexpression allowed the cells to stop dividing, re-specialize and resume their normal functions. 

When Artandi and Shkreli looked closely at the glomeruli in humans with HIVAN, they found that TERT expression was increased. Equally important, the Wnt signaling pathway, which is important in embryonic development and in the self-renewal of stem cells, was also activated. (Previous research in the Artandi lab has linked telomerase activity to the Wnt pathway.)  Blocking Wnt signaling in a mouse model of HIVAN also stopped the podocytes from dividing and improved their function. 

‘The implication is that podocytes may utilize recognized pathways of regeneration to renew themselves throughout life,’ said Artandi. People suffering from chronic kidney disease may simply have worn out or outpaced their podocytes’ capacity for renewal, he believes. 

Now that the researchers know podocytes have the ability [sic] regenerate in response to common cellular signals, their next step is to learn whether this regeneration occurs in healthy animals and people. ‘If we can harness this regeneration,’ Artandi said, ‘we may one day be able to treat people with chronic kidney disease.’” 

‘The URL for this article is  http://www.medindia.net/news/Hope-for-Treating-Chronic-Kidney-Disease-Via-Regeneration-of-Specialized-Cells-94388-1.htm 

That was then. Let’s see what more current info on podocytes tells us.  

This is from the September 2020 issue of Karger Journals which is a 131-year-old publisher of health sciences.  

“Podocytes are highly specialized cells located in the glomeruli, are incapable of undergoing mitosis [Gail again: this means splitting.] under normal conditions, and are mainly committed to avoid the loss of proteins in the urine. Their loss in the urine, defined as podocyturia, determines the appearance of glomerulosclerosis, proteinuria, and CKD. Podocyturia antedates proteinuria as a biomarker of kidney dysfunction, but at the present time, it is not a validated method to be employed in clinical grounds. Its main indication is to unravel the pathophysiological mechanisms of glomerular diseases.” 

Now I’m wondering why not? If podocyturia shows up before proteinuria, why allow it to progress to proteinuria? By the way, proteinuria is just what it sounds like: spilling protein in your urine instead of keeping it where it should be – in the blood. Is there no way to test for podocyturia? Is that the problem? 

But wait. I found this in a research paper by J. Bras Nefrol in the Brazilian Journal of Nephrology from back in 2013: 

“One of the assays used to assess podocyturia is indirect immunofluorescence with specific antibodies directed against podocyte antigens in urinary sediments.” 

This was in reference to lupus nephritis, but if the test can be used to detect one form of kidney disease, why not others? Of course, I’m not a doctor and have never claimed to be one. That’s important here because it explains that there is so much I don’t know that nephrologists do. I wish they’d explain why we can’t use this test for podocyturia. It might be able to prevent kidney disease. 

Until next week, 

Keep living your life! 

What the Heck is a Flozinator?

That’s the question I’ve been asking myself for weeks after seeing the term used on Twitter by such luminaries as Joel M. Topf, MD FACP [That means Fellow of the American College of Physicians.], The Nephrology Journal Club, nephrologist Swapnil Hiremath, and pediatric nephrologist Michelle Rheault, among others. First, I thought it was solely a nephrologists’ thing but hey, when has that ever stopped me? 

While the term is a new one, it’s traveled fast. It’s now accepted in the medical community. For example, this is the title of a paper published on PubMed, specifically on the National Institutes of Health’s National Library of Medicine’s National Center for Biotechnology Information site.   

“Biologically Plausible Trends Suggesting that Low-Protein Diet May Enhance the Effect of Flozination by SGLT2 Inhibitor Dapagliflozin on Albuminuria” 

Now we just need to know what the word means. While I couldn’t find a dictionary definition, I gathered from the twits [posts on Twitter] which I read that it means a doctor who uses empagliflozin, dapagliflozin and canagliflozin when treating a patient. Nice, so what are they? And how am I to explain in slightly under 900 words max? 

Let’s start with what I wrote about dapagliflozin on October 7th, 2019: 

“The obvious first stop to my way of thinking was Medline Plus, part of the U.S. Library of Medicine, which in turn, is part of the Institutes of National Health. 

‘Dapagliflozin is used along with diet and exercise, and sometimes with other medications, to lower blood sugar levels in patients with type 2 diabetes (condition in which blood sugar is too high because the body does not produce or use insulin normally). Dapagliflozin is in a class of medications called sodium-glucose co-transporter 2 (SGLT2) inhibitors. It lowers blood sugar by causing the kidneys to get rid of more glucose in the urine. Dapagliflozin is not used to treat type 1 diabetes (condition in which the body does not produce insulin and, therefore, cannot control the amount of sugar in the blood) or diabetic ketoacidosis (a serious condition that may develop if high blood sugar is not treated). 

Over time, people who have diabetes and high blood sugar can develop serious or life-threatening complications, including heart disease, stroke, kidney problems, nerve damage, and eye problems. Taking dapagliflozin, making lifestyle changes (e.g., diet, exercise, quitting smoking), and regularly checking your blood sugar may help to manage your diabetes and improve your health. This therapy may also decrease your chances of having a heart attack, stroke, or other diabetes-related complications such as kidney failure, nerve damage (numb, cold legs or feet; decreased sexual ability in men and women), eye problems, including changes or loss of vision, or gum disease. Your doctor and other healthcare providers will talk to you about the best way to manage your diabetes.’” 

[Could not find any attribute for this chart. Please let me know if you know the authors.]

Okay, got it. I’ll bet you do, too. On to canagliflozin. This is from my December 30th, 2019, blog: 

“I scooted over to EurekAlert! when I realized they were announcing a drug I’d blogged about: 

‘A drug like canagliflozin that improves both cardiovascular and renal outcomes has been eagerly sought by both patients with Type 2 diabetes and clinicians caring for them,’ added Kenneth Mahaffey, MD, professor of medicine at the Stanford University School of Medicine and co-principal investigator of the trial. ‘Now, patients with diabetes have a promising option to guard against one of the most severe risks of their condition.’ 

The researchers found the drug canagliflozin, a sodium glucose transporter 2 (SGLT2) inhibitor, was less effective at lowering blood sugar in people with reduced kidney function but still led to less kidney failure, heart failure and cardiovascular events such as heart attacks, strokes and death from cardiovascular disease. 

Professor Perkovic said the results were impressive. ‘The substantial benefit on kidney failure despite limited effects on blood glucose suggest that these drugs work in a number of different ways beyond their effects on blood sugar. This is an area of intense ongoing research.’”  

Notice that drug, just like the one before it and the one I’ll be writing about next end in ‘flozin.’ That should give you the biggest hint of what a flozinator does. 

Back to MedlinePlus

“Empagliflozin is used along with diet and exercise, and sometimes with other medications, to lower blood sugar levels in people with type 2 diabetes …. Empagliflozin is also used to reduce the risk of stroke, heart attack, or death in people who have type 2 diabetes along with heart and blood vessel disease. It is in a class of medications called sodium-glucose co-transporter 2 (SGLT2) inhibitors. Empagliflozin lowers blood sugar by causing the kidneys to get rid of more glucose in the urine. It is not used to treat type 1 diabetes (condition in which the body does not produce insulin and, therefore, cannot control the amount of sugar in the blood) or diabetic ketoacidosis (a serious condition that may develop if high blood sugar is not treated). 

Over time, people who have diabetes and high blood sugar can develop serious or life-threatening complications, includingheart [sic] disease, stroke, kidney problems, nerve damage, and eye problems. Taking medication(s), making lifestyle changes (e.g., diet, exercise, quitting smoking), and regularly checking your blood sugar may help to manage your diabetes and improve your health. This therapy may also decrease your chances of having a heart attack, stroke, or other diabetes-related complications such as kidney failure, nerve damage (numb, cold legs or feet; decreased sexual ability in men and women), eye problems, including changes or loss of vision, or gum disease. Your doctor and other healthcare providers will talk to you about the best way to manage your diabetes.” 

You may know this as the drug Jardiance. 

Notice all three are classified as SGLT2 inhibitors. I decided to take a look at the FDA’s website

“SGLT2 inhibitors are a class of prescription medicines that are FDA-approved for use with diet and exercise to lower blood sugar in adults with type 2 diabetes. Medicines in the SGLT2 inhibitor class include canagliflozin, dapagliflozin, and empagliflozin. They are available as single-ingredient products and also in combination with other diabetes medicines such as metformin. SGLT2 inhibitors lower blood sugar by causing the kidneys to remove sugar from the body through the urine. The safety and efficacy of SGLT2 inhibitors have not been established in patients with type 1 diabetes, and FDA has not approved them for use in these patients.” 

It looks like we’ve come full circle so it must be time to say goodbye. Wait! I almost forgot to mention that the Nephrology Journal Club is selling Flozinator merchandise. In their own words:

“We, at #NephJC, want to see SGLT2i blow-up and turn the tide in the war on chronic kidney disease. These drugs are amazing.

We also want to keep the work we do at NephJC moving forward and for that we need money. So we are putting these two goals together in the form of Merch!

Help us keep the #FOAMed flowing and tell the world that you are a FLOZINATOR!”

The address for merchandise is http://www.nephjc.com/flozinator. In addition to the mug, they also have pins and t-shirts. Doctors, are you listening?

Until next week, 

Keep living your life! 

Pleasant Dreams

I have Sleep Apnea and so do many of you. I used a mouth guard for years. Once that stopped working for me, I switched to a BiPap, but wasn’t too happy with it. Quick reminder: BiPap means Bilevel Positive Airway Pressure or your prescription air pressure breathing in and a lighter air pressure breathing out.

My hair was always flattened, and I was always tired. I needed something that wouldn’t leak and had no head straps, but what? Then I discovered DreamPort. Since Sleep Apnea can affect your Chronic Kidney Disease and your Diabetes, and even your high blood pressure, I knew I had to share this new information with you.

Stuart Heatherington, the Founder and Executive Chairman of Bleep, LLC jumped to when I asked him to write a guest blog about his product. While this is not an advertisement for DreamPort, I do recommend it for those with Sleep Apnea who are having problems with mask leakage and/or are just plain tired of flattened hair and lines on their faces.

“Sleep Apnea is when a person stops breathing as they sleep, and it can happen hundreds of times a night. The person’s airway closes from as little as a few seconds to longer than a minute in severe cases. In order to start breathing again, you are jarred awake to break the obstruction with loud snoring and gasping for breath. Sleep Apnea disrupts normal restful sleep waking the individual up from 10/hr. to as much 150/hr., leaving the sufferer tired and stressed, and, if untreated, at a much higher risk of heart attack, stroke, kidney ailments, hypertension, blood sugar spikes, car accidents, memory issues, etc.

I’m sure many of you know a family member or friend suffering from Sleep Apnea, if you do not suffer from Sleep Apnea yourself. Almost everyone knows someone that falls asleep at family get-togethers or the second they sit in a car as a passenger.

The gold standard for treatment is called CPAP or APAP therapy. With this therapy a PAP machine uses room air to keep the airway open and prevent it from collapsing and causing an obstructive apnea. PAP therapy has been around for decades and is proven to effectively treat obstructive Sleep Apnea. However, many patients struggle with PAP therapy and it is largely due to the comfort of the mask.

There are hundreds of FDA approved CPAP masks on the market, and they all have one thing in common – the mask is held in place with headgear and straps. The issue with headgear is that although it holds the mask in place, it does not prevent leaks. Leaks occur when the seal between the mask and face/nose is broken, and air leaks out. The fix for the leaky mask is to tighten the headgear and mask on your face. This fix then leads to many other issues that trouble CPAP users such as lines on the face that last for hours, skin irritation and breakdown on the nose and in the nose, matted and damaged hair. Those are just a few examples. So, you can see how many CPAP users struggle with the therapy, to the point that some give up. The Bleep DreamPort Sleep Solution is different in that we do not use headgear, and we do not leak.     

The DreamPort is adhered to the nose using hypoallergenic surgical foam tape [Gail here: I have not had any problems with the adhesive.] to create a night-long leak-free seal. It’s Latex-Free, BPA-Free, Corn-Free and Silicone-Free on the seal. Because the tape adheres directly to the nose, there is no leak, and because there is no leak and no headgear, there is nothing to tighten. All the issues I previously mentioned just go away.

DreamPorts are nightly disposable, so each night the individual gets a fresh new set of DreamPorts to apply. Since we are different from traditional CPAP masks, it is very important that the instructions are carefully read, or the instructional video is watched to ensure proper use. It is also important to clean your nose area prior to applying the DreamPorts with an astringent such as Witch Hazel or Alcohol, as soaps have oils and moisturizers in them that can impact the ability of the adhesive to stay on all night.

Because there is no leak and no headgear, the individual can sleep in any position. With a standard CPAP mask and traditional headgear, whenever the individual rolled over on their side, the pillow pressed up against the mask and caused a leak. This leak would wake up the individual. Because DreamPort seals so well, the pillow will not cause a leak and the individual can sleep in any position.     

I am a Sleep Apnea sufferer myself and have experienced all the issues most people have with Sleep Apnea. A number of years back, while traveling to a CEU conference, I woke up at 3AM with an epiphany. I jotted down the idea on a napkin and woke my wife up to talk about it until 5 a.m. That was a Saturday morning. We drove home Sunday after the show.

I went straight to Lowes and CVS and bought the items needed to put the proof-of-concept together. I took my old CPAP mask and reconfigured it using copper tubing from Lowes and corn patches bought at CVS and an older product called Provent that used a tape similar to our needs. Although the initial design was a bit crude, it worked all night at a pressure of 10 centimeters of pressure. On Monday morning I started the work of hiring a patent attorney and hired an engineer a couple days later to help with concept design. 

End result? You can find us on www.bleepsleep.com or visit our Facebook page at BleepSleep.”

I have no reservations about endorsing this product. How very nice to be able to sleep on my side again if I want to. How very nice to actually get a good night’s sleep again. Thank you for that, Stuart.  

What’s That Sound I Hear?

My husband suffers from tinnitus and often complains about how loud “the crickets” are. He tells me there’s nothing that can be done about this. But then, a reader asked about tinnitus, and I realized chronic kidney disease patients have a three time more likelihood of developing this malady. Now I can no longer accept that nothing can be done. 

Photo by Dane Sam on Pexels.com

Let’s start at the beginning. Just what is this? Oh goody, time to consult my favorite dictionary. That, of course, is The Merriam-Webster

“a sensation of noise (such as a ringing or roaring) that is typically caused by a bodily condition (such as a disturbance of the auditory nerve or wax in the ear) and usually is of the subjective form which can only be heard by the one affected” 

Wait a minute. That doesn’t say anything about chronic kidney disease. But a large study published by The National Center for Biotechnology Information [(NCBI] does:  

“This study presented that CKD is a significant and independent risk factor for tinnitus. The patients with CKD have a 3.02 times higher risk of developing tinnitus. Furthermore the patients with end stage renal disease and dialysis are at a 4.586 times risk of tinnitus than general population and carry a higher risk of tinnitus than the patients with CKD and without dialysis….”   

The NCBI is part of the United States National Library of Medicine [NLM], which is a branch of the National Institutes of Health [NIH].    

Everyday Health tells us what the causes of tinnitus may be: 

“Tinnitus is often associated with high blood pressure, allergies, and abnormal kidney function. Tinnitus can also occur because of: 

Tumors 

Cardiovascular problems 

Medication side effects 

Loss of hearing 

Being around very loud noises 

A head or neck injury 

Bones in the middle ear that become harder” 

 
Did you notice “high blood pressure” and “abnormal kidney function” in the explanation above? By the way, my husband had been around very loud noises the whole time he served in Vietnam.  

I found a highly readable explanation on the connection between the kidneys and ears at Hearing Unlimited. 

“If you asked a medical professional about the kidneys and the ears, they would tell you that ‘the kidneys share physiologic, ultrastructural and antigenic similarities with the stria vascularis of the cochlea.’ Or, in plain English: a specific part of our ears shares functional and structural characteristics with our kidneys. 

Photo by Hassan OUAJBIR on Pexels.com

It almost sounds unreal – how could the ears share similarities with the kidneys? But research has confirmed that physiological mechanisms of fluid and electrolyte balance are present in both organs. This matters because it means that when a health issue affects the functionality of one (i.e. the kidneys or the ears), it’s likely to affect the other ….” 

Now what? It’s there. You have CKD, but you don’t know if that’s the cause of your tinnitus. WebMD has some suggestions that may or may not work, but they seem worth a try… except for those you just can’t try because you have CKD. For example, I’d stay away from the herbals because they aren’t regulated. Do check any other medications with your nephrologist before you proceed. 

“Even if a specific cause is never found, there is still hope for successful treatment. A combination of therapies over time usually offer the best hope. 

Biofeedback, relaxation training, counseling, and individualized psychotherapy helps manage stress and helps you change your body’s reaction to the tinnitus. Tinnitus Retraining Therapy (TRT) combines counseling with special background sounds designed to help people suppress the sounds of their tinnitus. 

Antianxiety medications, such as Valium or Xanax, as well as a wide range of antidepressant medications, are very helpful for tinnitus sufferers. Other medications, such as diuretics (water pills), muscle relaxants, anticonvulsants medications, and antihistamines, are also used. 

Special hearing aids, electronic masking devices, or both, are often used when other methods have failed to achieve control. Cochlear implants and cochlear stimulation devices are being investigated for severe, intractable tinnitus cases. Surgical injections of lidocaine directly into the inner ear are also being used in some cases. 

Alternative treatments such as hypnosis, acupuncture, chiropractic adjustments, vitamin/mineral supplements, and herbal remedies may have some promise, but there is little, if any, meaningful research as to their effectiveness. Ginkgo biloba — which is being studied to determine its effectiveness for tinnitus — is said to improve blood flow and nerve function. Use ginkgo biloba with caution if you have a bleeding disorder or take blood thinners. Explore alternative options carefully, with the cooperation of your medical providers.” 

That got me to wondering if lifestyle changes could be of any help. Bingo! Hearing Associates of Las Vegas suggests you avoid the following: 

“Smoking 

Caffeine consumption 3 hours before bed 

Drink more water and less other liquids 

Any food triggers 

Listening to media at high settings” 

Photo by Andrea Piacquadio on Pexels.com

Avoiding smoking and drinking more water are two suggestions that would help your CKD even if you didn’t have tinnitus. 

I got curious about the special hearing aids since that’s something we hadn’t tried for my husband. In attempting to research that, I discovered something called a masker.  

“A tinnitus Masker is an electronic hearing aid device that generates and emits broad-band or narrow-band noise at low levels, designed to mask the presence of tinnitus. 
 
Such masking noise is also referred to as white noise. For an individual suffering from both hearing loss and tinnitus, the masker and the hearing aid can operate together as one instrument.” 

This information is from Hear-It. I thought you might think they were a selling site [as I did], so I’m including this information from their website: 

“Hear-it.org is a non-commercial web site and has been established to increase public awareness of hearing loss. Hear-it.org is one of the world’s leading and most comprehensive websites on hearing, hearing loss and tinnitus and how to treat and live with hearing loss or tinnitus.” 

Until next week, 

Keep living your life! 

A New Pregnancy and a New Diagnose

I have two grandsons. One is three and a half. The other is 21 months. How do I explain to them what my life is like if I go on dialysis? Or require a transplant? Sure, I’m a writer… but not for children. That’s a special kind of author. That’s why I asked Jessica Webb, a Christian children’s book writer, if she wouldn’t mind explaining how she came to write a kidney disease book for children. She was kind enough to guest blog to clue us in on her particular journey. Here’s what she wrote:   

I was always aware that I was different from other kids my age for as long as I can remember. But it wasn’t until I was pregnant that I found out something wasn’t right. A 24 hour urine test came back with a very high protein count. That was the beginning of a new chapter in my life. 

I was referred to one of the top nephrologists in Louisville, Kentucky when I was about four months pregnant. To my dismay, my pregnancy was now considered high risk. I was informed I had some sort of kidney disease, but a biopsy could not be performed until after I had the baby.   

We continued routine OB/GYN appointments, nephrology appointments, and high-risk OB/GYN appointments.  Around 35 weeks, my creatinine was close to 2.5. My doctor panicked and said the baby had to be born before there was more kidney damage. That started 48 hours of hell.  

I was pumped full of magnesium because I’d had a few bouts of high blood pressure. The medical staff assumed I had preeclampsia. Magnesium sulfate was protocol for preeclampsia. I felt paralyzed and everything was blurry. I started having very, very low blood pressure, was throwing up, and came close to passing out.  

The morning after my son’s birth, I awoke feeling sick. I still was nearly blind and could not move a muscle. I told my husband something was amiss, and they have to stop giving me this magnesium ASAP. 

My husband and I don’t like conflict. We try to trust doctors and nurses. We never had a reason not to. But I told my husband if something doesn’t happen, I’m going to die. “Get me the nurse now!” I yelled.  

For the first time in my life, I was aggressive towards the nurse because she wasn’t listening to me. I told her to stop the magnesium right away. She did. A few hours later, a nephrologist arrived who said, “Thank God, you told them to stop the magnesium because it was eight on the 1-10 magnesium scale. Nine is when most people go into cardiac arrest.”  

The nurses had also given me Advil and Motrin for pain and that made my creatinine skyrocket. I learned during that hospital stay how differently we have to treat our bodies as people with kidney disease. Our bodies do not react the same way as non-kidney patients’ bodies do.   

Once I was discharged from the hospital and then my son was a month later, I started my journey of finding out what my kidney disease was caused by. We did a biopsy. The nephrologist told me there had been no doubt in his mind I had FSGS. Then began the extensive researching, reading, and asking questions about this disease. I learned that even with a transplant, FSGS can come back in the new transplanted kidney. I was devastated. 

What really helped me get through those months was that I started to illustrate and write children’s books. I wrote two Christian based books over those months and sold a lot to friends and family.  

I knew what my third children’s book had to be. I wanted to write a book about kidney disease, dialysis, and transplant. I wanted it to be light-hearted and funny, so young children could understand the seriousness of the situation. If they had a family member on dialysis, I wanted to explain to them why this person didn’t always feel healthy enough to participate. Or, if they were the ones on dialysis or had to have a transplant, to give them ways to cope. I also wanted to show preventive ways to take care of your kidneys and give more information on the subject in general.  

When I looked around to see if there was anything like that when my son was little, I couldn’t find anything. He learned the hard way. But I would have given anything to have a book to help his little mind understand the gravity of the situation. My book, The Book About Kidneys: And No, Not the Beans, has been a hit with the dialysis community. I’m so glad to be offering this resource to the little ones in our lives.   

Three things I wish I’d known before this all happened: 

One – I wish someone had told me to take a breath and get a second or even third opinion.  

Two – YOU are the only true advocate for yourself and your health. Doctors only know what they’ve seen before or what they’ve studied. But this is a very complex disease, and all of our bodies are different. Don’t let anyone brush off a symptom they say is unrelated.  

Three – If you aren’t the one on dialysis but your loved one is, be patient with them. This disease is a nasty one. One day they may not feel too bad and the next may be their worst day. Love them and be kind. Don’t just ask them how you can help. Take it upon yourself to do so.  

I hope to release more books on the subject of kidney disease and major illness. You can find my books on Amazon. Thanks! Jess 

While the book does have a bit of a Christian bent, I found it well worthwhile for children. It’s fun and informative without being overwhelming to “little minds.” I’m a bit relieved that there is a book to explain to my grandsons should that be necessary. 

Until next week, 

Keep living your life! 

Uh, What’s That?

 Finally, a bunch of help for slowing down chronic kidney disease! The latest one that caught my eye was Kerendia. It was the spelling that grabbed me. [Remember: I am a former English teacher.] This is the announcement from diaTribe

“On July 9, the FDA approved the drug KERENDIA (finerenone) which has been shown to slow the progression of chronic kidney disease (CKD) that is associated with type 2 diabetes. This new medication is indicated to reduce the risk of eGFR decline, kidney failure, cardiovascular death, non-fatal heart attacks, and hospitalization for heart failure – which are all associated with CKD as a result of having type 2 diabetes.” 

DiaTribe is new to me and you, so here’s what they have to say about themselves: 

“At The diaTribe Foundation, we believe that the millions of people living with diabetes, prediabetes, and obesity today deserve education and support to help them manage their health. 

Through our publication, diaTribe, we provide readers with cutting-edge diabetes insights and actionable tips that empower them to manage their diabetes. In doing so, we hope to help people become happier and healthier.” 

To say the least, this is ‘cutting-edge’ news. But why the two different names? The drug company that developed the drug – Bayer – uses Kerendia as its brand name, a common practice for drugs. For example, you’re probably familiar with aspirin [which is a NSAID, so don’t take it if you have CKD.]. That’s a brand name. The actual name for aspirin is acetylsalicylic acid. Just so, Kerendia is the brand name for finerenone. 

I have to admit I simply had no clue as to what finerenone is. So, I did what I always do. I looked it up.  It turns out that finerenon is a non-steroidal mineralocorticoid receptor antagonist. Wonderful. That didn’t help me in the least. 

Let’s go bit by bit. We do know that non-steroidal isn’t good for CKD patients. Time to hit the dictionaries. The Freedictionary’s Medical Dictionary tells us it means: 

“Not containing steroids or cortisone. Usually refers to a class of drugs called Non Steroidal Anti-Inflammatory Drugs” 

Do you remember why we can’t take NSAIDS? I enjoyed the easily understood answer to this question from Ochsner Health. They are one of the top hospitals in the USA. 

“NSAIDs can affect kidneys by several different mechanisms. They can cause high blood pressure and can also interact with some blood pressure drugs in a way that prevents them from working correctly such as diuretics, ACE inhibitors, and ARBs which are a group of drugs that are designed to relax blood vessels. NSAIDs may increase your fluid retention and can lead to decreased blood flow to kidneys. This is because NSAIDs block prostaglandins, which are the natural chemicals that dilate blood vessels and allow oxygen to reach the kidneys to keep them alive and healthy.” 

Got it. On to mineralocorticoid. The same dictionary as previously used tells us that it means: 

“Hormones from the outer layer (cortex) of the adrenal gland that promote retention of sodium and excretion of potassium in the urine.” 

And here we are trying our darnedest to avoid sodium and potassium. I think we can figure out both receptor and antagonist by ourselves. Add all this together and we find that non- steroidal mineralocorticoid receptor antagonist is not a NSAID but does prevent the introduction of certain hormones that make our sodium and potassium levels worse. I think. That wasn’t so hard, was it? [She asked tongue in cheek.] 

Now that we know what it is… sort of, let’s find out if there are side effects. Most drugs have them. I turned to my trusty old pal, RxList

Photo by Lisa A on Pexels.com

“Side effects of Kerendia include: 

high blood potassium (hyperkalemia),  

low blood pressure (hypotension), and  

low blood sodium (hyponatremia).” 

This is important to know because, as WebMD explains: 

“The body needs a delicate balance of potassium to help the heart and other muscles work properly. But too much potassium in your blood can lead to dangerous, and possibly deadly, changes in heart rhythm.”  

As for hypotension, The MayoClinic has that one covered: 

“Even moderate forms of low blood pressure can cause dizziness, weakness, fainting and a risk of injury from falls. And severely low blood pressure can deprive your body of enough oxygen to carry out its functions, leading to damage to your heart and brain.” 

And, finally, hyponatremia. Healthline, that wonderful company that awarded this blog not one, but two, awards tells us: 

“Sodium is an essential electrolyte that helps maintain the balance of water in and around your cells. It’s important for proper muscle and nerve function. It also helps maintain stable blood pressure levels.” 

I also noticed on a few sites that grapefruit or grapefruit juice can make the occurrence of side effects more frequent. There are other, less common side effects of kerendia. 

Keep in mind that this drug is only for those who have Chronic Kidney Disease and type 2 Diabetes. I think that calls for a little refresher. Type 1 Diabetes is when you don’t produce insulin. Type 2 is when you produce insulin, but your body is resistant to using the insulin you produce. Insulin is: 

“a protein pancreatic hormone secreted by the beta cells of the islets of Langerhans that is essential especially for the metabolism of carbohydrates and the regulation of glucose levels in the blood and that when insufficiently produced results in diabetes mellitus” 

Great! I got to use my favorite dictionary, The Merriam-Webster, for that definition.  

Personally, I am no longer pre-diabetic since two thirds of my pancreas have been removed due to cancer. Unfortunately, it’s because I am now a Type 2 Diabetic. You can’t have all the pancreatic hormone you need if you only have one third of your pancreas. 

Some blogs come easy; some don’t. This one didn’t. I hope it helps you understand this new drug so you don’t have to research it yourself. 

Until next week, 

Keep living your life! 

What It’s Like To Be A Kidney Donor

Last week I’d mentioned that I don’t have any first hand experience as a kidney donor, but knew someone who did. Although I know she’s pretty busy with her business, I took a chance and asked her if she’d like to guest blog about her experience as a kidney donor. Amy Donohue responded practically before I hit send. She was ready, much more than willing, and able to do just that. I had her guest blog in my hands within a day. As Amy says, “I love spreading the gospel of live organ donation.”

Ladies and gentlemen, this was Amy’s experience.

“I’ll do it. I’ll donate my kidney. What do I have to do?

Amy and TinyMom

That was a Friday night tweet from me in January, 2011, to a Twitter follower whose mother finally agreed to be put on the transplant list at Mayo Clinic. I saw a conversation between two people I had been following for a few years and responded.

I started testing as soon as I learned the process, and it started with a blood test to see if our blood types matched closely enough for me to be able to donate. My recipient, TinyMom, emigrated to the States in the 70s. Her kidney failure had been caused by high amounts of ibuprofen for a migraine. I lost my father to cancer, and couldn’t help in any way at all, which prompted me to help her.

My testing had to be spread out over a couple months because I’m a single woman, living alone, and I had had, at the time, a fairly new job. I kept track of all appointments to give to my bosses and maintain transparency about my testing and donating. I tried to do as many tests at once as possible, and spent Valentine’s Day 2011 at the Mayo Clinic in North Phoenix. 

The first test that day was a pregnancy test. When someone wants to donate, tests have to be thorough because there can be no harm to the donor, and they need to make sure we are healthy enough to not only donate, but make it through a 90-minute surgery. Next, I had to give several vials of blood. The third appointment that day was with an advocate. For donors, transplant centers want to be sure donors are advocated for and taken care of. I also had to see a social worker and psychiatrist, to make sure my intentions were pure. I had a mammogram, CT scan, and gave more blood and urine during the testing process.

I wanted nothing out of this but to help a woman have a better quality of life. Due to the whole process starting because of a tweet, though, I also had to do media interviews. I wanted to do them to educate others who may be interested in donating. The more open I was about testing, the more I hoped others would follow suit and do what I was doing. The interviews were exhausting for me, because not only was donating a kidney on my mind 24/7, but it also invited a lot of negativity. Thankfully, I had a ton of community support to get through it. I still hadn’t even met TinyMom, until we had our local FOX affiliate interview all of us together.

Two weeks before the scheduled surgery, I was fired from my job for missing my sales goal due to testing. Thankfully, the following morning, a Twitter follower hired me, and I started working immediately. I couldn’t be unemployed for the couple of weeks leading up to the surgery, because then I would have nothing to do but think about what was coming. I was tired of thinking.

The Today Show came out twice to interview us, and were there as we were being wheeled into the operating room. My last words: “Get that f**king camera out of my face!” (Sorry for the language!) All I wanted was to get this kidney out of me and into her, so she could be there for her family, and here I was, in a hospital gown all doped-up but still having a camera in my face. At this point, I wanted that anesthesia so I could have a break for a couple hours. I was exhausted mentally and emotionally. It was April 19th, 2011.

As I was being prepped for surgery, the surgeon noticed a potential problem. When they had given me a CT scan to decide which kidney to take, they had to make sure TinyMom had the same number of veins and arteries going to and from the kidney. They decided on my right kidney, which is rare, because it seemed like the best match.

When they cut me open, though, they realized I had had an extra renal vein that didn’t show up on the CT scan. My team of surgeons immediately spoke with TinyMom’s team, explaining there could be a potential problem. They had just finished prepping her for surgery.

Their response: “You’re not gonna believe this, but SHE has the SAME renal vein that didn’t show up on her CT scan!” 

This was meant to be. 

When I heard about it after waking up in my room, I cried. It was finally over, and we had a connection that was even deeper than I had thought. 

I was up and walking around within an hour or two of getting to my room. The more we walk after surgery, the quicker we heal and can go home. My stay was about 48 hours. I was walking around the nurses station by the evening of my donation. I was feeling great! 

I was out of the hospital in 48 hours, and got home on a Thursday. I was at my desk working the next day. The worst part of the recovery was the constipation from the anesthesia. I was hiking within 3 weeks of surgery, and could have sex around that time, too. Since they removed my kidney where women have a C-section, I just had to wait for the swelling of my abdominal muscles to ease before resuming normal physical activities. 

It’s been ten years now, and I am healthier than I have ever been. I haven’t seen TinyMom for awhile, due to the pandemic, but we will get together soon. We talk on the phone a lot and really miss each other. We have a deep connection, made deeper by a 3-ounce organ.”

Thank you, Amy. Now we know. 

Until next week,

Keep living your life!

 

The Other Side of the Coin

We are having an extreme heat warning here in Arizona. For us, that means we stay in the air conditioned house. For some reason, that makes me very eager to write. I’m working on a book about my dance with cancer, a sequel to Portal in Time (or maybe a prequel), and a murder mystery. But, of course, the blog comes first. This is my payback for everything good that’s ever happened to me. 

Last week, I wrote – without going too deeply into the topic – about obtaining a kidney. This week I’ll be writing about donating a kidney. I have it in mind to ask a friend who is a kidney donator about writing a guest blog, but we may have to wait a bit for that. She is one busy person. 

So, without this first-hand experience, let’s see what we can find out. According to the National Kidney Foundation, living donation can come from the following: 

“Living donation takes place when a living person donates an organ (or part of an organ) for transplantation to another person. The living donor can be a family member, such as a parent, child, brother or sister (living related donation). 

Living donation can also come from someone who is emotionally related to the recipient, such as a good friend, spouse or an in-law (living unrelated donation). Thanks to improved medications, a genetic link between the donor and recipient is no longer required to ensure a successful transplant. 

In some cases, living donation may even be from a stranger, which is called anonymous or non-directed donation.” 

But not everyone can donate a kidney. I turned to Dignity Health, the fifth largest health system in the nation, for more information about not being able to donate: 

“Living donors should be in good overall physical and mental health and older than 18 years of age. Some medical conditions could prevent you from being a living donor. Medical conditions that may prevent a living kidney donation may include uncontrolled high blood pressure, diabetes, cancer, HIV, hepatitis, acute infections, or a psychiatric condition requiring treatment. Since some donor health conditions could harm a transplant recipient, it is important that you share all information about your physical and mental health. 
 
You must be fully informed of the known risks involved with donating and complete a full medical and psychosocial evaluation. Your decision to donate should be completely voluntary and free of pressure or guilt.” 

So now that we have an idea of who can and who cannot donate a kidney, the original question remains. How do you donate? 

The most logical source I could think of for this information was The American Kidney Fund. Here’s what they had to say: 

“Contact the transplant center where a transplant candidate is registered. 

You will need to have an evaluation at the transplant center to make sure that you are a good match for the person you want to donate to and that you are healthy enough to donate. 

If you are a match, healthy, and willing to donate, you and the recipient can schedule the transplant at a time that works for both of you. 

If you are not a match for the intended recipient, but still want to donate your kidney so that the recipient you know can receive a kidney that is a match, paired kidney exchange may be an option for you. 

Another way to donate a kidney while you are alive is to give a kidney to someone you do not necessarily know. This is called living non-directed donation. If you are interested in donating a kidney to someone you do not know, the transplant center might ask you to donate a kidney when you are a match for someone who is waiting for a kidney in your area, or as part of kidney paired donation. You will never be forced to donate.” 

Let’s take a look at the actual procedure now. The most commonly used surgical procedure for kidney donation is laparoscopic. The University of California San Francsico explains it far better than I could: 

“Laparoscopic donor nephrectomy is minimally invasive surgery that utilizes instruments such as a camera (videoscope) and tools (instruments) to remove the kidney on long, narrow rods that are placed into the abdomen through small incisions. 

The videoscope and surgical instruments are maneuvered through three or four small incisions in the abdomen. Carbon dioxide is pumped into the abdominal cavity to inflate it, which helps the surgeon to see and maneuver better.  

Once the kidney is freed, it is secured in a bag and pulled through an incision that is about 3 inches long and is several inches below the umbilicus (belly button).  

Laparoscopic donor nephrectomy has several benefits over open nephrectomy, including faster recovery time, shorter hospital stay, and less post-operative pain.  The majority of transplant centers today perform laparoscopic donor nephrectomy for their living donors.” 

Finally, let’s find out what life would be like for you after donating your kidney. 

“You will need a few weeks to months to heal from surgery, but after that most donors are able to return to their normal daily life: 

You won’t need lifelong medicines 

You can eat the same things you did before donation 

You can be active and play sports 

You can still get pregnant or father a child 

Most living donors say they were happy with the donation experience and that they would do it again. It’s a chance to change someone’s life. In a few cases, related living donors have even reported an improved quality of life after donation. 

To stay healthy, you’ll need medical checkups yearly and need to stay at a healthy weight after donating.” 

Thank you to UNOS [United Network for Organ Sharing] for the above information. 

I think I just may have become a kidney donor myself if I didn’t have diabetes. In any case, I did find this fascinating. It’s one of those things I’ve always wondered about and promised myself that I would find out about some day. Someday has come and now we both know a bit about being a kidney donor. 

Until next week, 

Keep living your life!  

There is Help

You may have noticed that I ‘steal’ most of my Facebook transplant posts from Jim Myers, better known in the kidney community as Uncle Jim. As kidney disease advocates, we are a very sharing bunch. You may have figured this out yourself when you read all the guest blogs while I was dealing with pancreatic cancer. Jim’s guest blog was on March 23, 2020. Use the archives dropdown to the right of the blog if you’d like to re-read the guest blogs mentioned today. 

I used to write in the foreword to the SlowItDownCKD book series that I didn’t deal with transplant because I didn’t know much about it. I think it was really because the thought any major surgery scared me. After two of my own during the cancer dance, I’m not afraid to write about transplants. Again, you’ve probably figured that out yourself by the number of transplant blogs in the last few years. 

While I’ve explained what a transplant is , why it’s needed, what kinds of kidneys can be used [4/19/21’s blog], and how the operation is executed [4/26/21’s blog], I have not written anything yet about help in finding a kidney. That’s where today’s blog comes in. Now keep in mind that this is not the only way to obtain a kidney, but it is a big help. 

The Resources & Services Administration’s Data Warehouse, a part of the Department of Health and Human Services, offered some numbers for us. Last year in the U.S. alone, there were 92,036 patients [about the seating capacity of the Los Angeles Memorial Coliseum] waiting for a kidney transplant. Only 21,656 received one. I decided to include kidney/pancreas transplants, too. 1,579 patients needed this double transplant, but only 674 received it. I am not a numbers person, but even I found this astounding. Look at the disparity between those people needing a kidney transplant and those receiving one. 

The American Kidney Fund offered quite a bit of information about getting on the national organ waiting list: 

“The process of getting listed for a kidney transplant often begins when your doctor refers you for the transplant surgery. But, you do not have to be referred by a doctor. You are free to visit a transplant center to be evaluated if you are interested in transplant. 

You can only be ready for a kidney transplant after you have passed the required evaluation at a transplant center that looks at your physical health, mental health, and finances. If you pass this evaluation and the transplant team decides you are ready for transplant, you will be added to the national waiting list. 

The national organ waiting list is managed by an organization called the United Network for Organ Sharing (UNOS), a private, nonprofit agency that works with the federal government. UNOS keeps track of all the people in the United States who need kidney transplants, and matches them with donors. 

The national waiting list is not an ordered list that gives priority to the person who has been listed the longest. The UNOS waiting list uses complex ways to calculate where and when the best kidney match becomes ready for you. 

The United States is divided into 11 regions and 58 local Organ Procurement Organizations (OPO)s, which are areas used to find matches for transplant. For example, if a kidney becomes available, UNOS will first try to find a match in the OPO where the kidney is being donated. If no match is found there, UNOS will search within the larger region. If no match is found within the OPO or region, the kidney will then be available to someone who lives outside the region. 

When deciding who gets an available kidney, UNOS considers things about the donor and the person who is getting a kidney (the recipient): 

The age of the recipient 

Blood type of the donor and recipient 

The size of the donor kidney compared to the body of the recipient 

How urgent it is for the recipient to get a kidney 

How long the recipient has been waiting for a kidney 

The distance of the recipient from the donor kidney” 

 
There’s also something called a kidney exchange or swap. UCLA Health explains what this is: 

“What is a Kidney Swap? 

If a donor and recipient have a different blood type, they can exchange their kidneys with another donor and recipient pair in a similar situation. 

This can also be done among three pairs.” 

I turned to the Mayo Clinic to find out if there are people who would not be eligible for a kidney transplant: 

“But for certain people with kidney failure, a kidney transplant may be more risky than dialysis. Conditions that may prevent you from being eligible for a kidney transplant include: 

Advanced age 

Severe heart disease 

Active or recently treated cancer 

Dementia or poorly controlled mental illness 

Alcohol or drug abuse” 

Uh-oh, is 74 considered advanced age? Is a year and a half ago recently treated cancer? I am so glad I’ve been able to keep my GFR in the low 50s. 

There is another kind of kidney transplant. That is preemptive. As Uncle Jim [Hi again, Jim!] wrote on the National Kidney Foundation’s website: 

“A preemptive kidney transplant is a transplant that takes place for a kidney patient, before starting dialysis. It usually takes place before your kidney function deteriorates to the point where you need dialysis. In the U.S., only 2.5% of all kidney transplants are preemptive. Preemptive transplants are considered to be the preferred method of transplants when compared to post-dialysis transplants.” 

Kevin Fowles guest blogged about his preemptive kidney transplant in March 16, 2020’s blog. There’s much, much more information you’ll need to know about kidney transplants if you need one or even if you’re just interested. I think to cover all the information I’d have to blog about them for several weeks.

I wanted to give you a gentle introduction to the different kinds of kidney transplants there are and how to start obtaining one. There is a wait… a long wait. So be prepared. Speak with your nephrologist to start the process or for questions particular to your kidney disease. You can always ask me general questions about transplants, and I’ll try to answer them for you. Keep in mind that I’m not only NOT your doctor, I’m not a doctor at all. 

Until next week, 

Keep living your life! 

It’s All Connected

With Mother’s Day last month and Father’s Day this month, I’ve been thinking about family a lot. Basically, I’ve been wondering if there are any oblique links to chronic kidney disease for any members of my family. As I ruminated, one link popped up. One of my daughters has PCOS… and has recently been diagnosed with diabetes… which we know is the primary cause of CKD. Uh-oh. 

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Let’s see how this all works. We know that CKD is the progressive decline of your kidney function for at least three months. We know that diabetes is either not producing insulin, which is type 1, or being unable to make use of the insulin you do produce, which is type 2. By the way, I’m type 2 but that was diagnosed many years after the ckd was diagnosed for me. CKD is also a prime cause of diabetes. It works both ways: CKD can cause diabetes and diabetes can cause CKD.  

And PCOS? Each time, my daughter tells me about it I have to ask, “Uh, what is that again?” PCOS is polycystic ovary syndrome. Big help, huh? Thank goodness for a more thorough answer from my old buddy TheMayoClinic

“Polycystic ovary syndrome (PCOS) is a hormonal disorder common among women of reproductive age. Women with PCOS may have infrequent or prolonged menstrual periods or excess male hormone (androgen) levels. The ovaries may develop numerous small collections of fluid (follicles) and fail to regularly release eggs. 

The exact cause of PCOS is unknown. Early diagnosis and treatment along with weight loss may reduce the risk of long-term complications such as type 2 diabetes and heart disease.” 

I wondered if my daughter knew something was amiss or if her doctor picked this up, so I did the usual – looked up the symptoms. I found John Hopkins Medicine the most helpful source for this information: 

“The symptoms of PCOS may include: 

Missed periods, irregular periods, or very light periods 

Ovaries that are large or have many cysts 

Excess body hair, including the chest, stomach, and back (hirsutism) 

Weight gain, especially around the belly (abdomen) 

Acne or oily skin 

Male-pattern baldness or thinning hair 

Infertility  

Small pieces of excess skin on the neck or armpits (skin tags) 

Dark or thick skin patches on the back of the neck, in the armpits, and under the breasts” 

Wait a minute. This is not that clear. Where does the insulin part of PCOS come in? That’s what is responsible for diabetes and diabetes is the foremost cause of CKD. Webmd explains: 

“Your body makes hormones to make different things happen. Some affect your menstrual cycle and are tied to your ability to have a baby. The hormones that play a role in PCOS include: 

Androgens. They’re often called male hormones, but women have them, too. Women with PCOS tend to have higher levels. 

Insulin. This hormone manages your blood sugar. If you have PCOS, your body might not react to insulin the way it should. 

Progesterone. With PCOS, your body may not have enough of this hormone. You might miss your periods for a long time or have trouble predicting when they’ll come.” 

Aha! So PCOS interferes with your insulin… which is practically the definition of insulin. MedicalNewsToday confirms this in describing the three major types of diabetes: 

“Type I diabetes: Also known as juvenile diabetes, this type occurs when the body fails to produce insulin. People with type I diabetes are insulin-dependent, which means they must take artificial insulin daily to stay alive. 

Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity. 

Gestational diabetes: This type occurs in women during pregnancy when the body can become less sensitive to insulin. Gestational diabetes does not occur in all women and usually resolves after giving birth.” 

Let’s move on to how diabetes can cause CKD, just in case you’ve forgotten. The National Institutes of Diabetes and Digestive and Kidney Diseases, which is part of the National Institutes of Health, which is part of the U.S. Department of Health and Human Services is of service here: 

“High blood glucose, also called blood sugar, can damage the blood vessels in your kidneys. When the blood vessels are damaged, they don’t work as well. Many people with diabetes also develop high blood pressure, which can also damage your kidneys….” 

Remember, it’s your insulin that controls the amount of blood glucose you have. Without producing insulin or if your body doesn’t respond well to insulin, you have diabetes. If you have diabetes your kidneys’ blood vessels may be damaged and you may ‘develop high blood pressure,’ which is a major cause of CKD. 

High blood pressure is actually the second most likely cause of CKD. So, it seems that PCOS can lead to diabetes which may lead to high blood pressure, the latter two both major causes of CKD. It seems to me that I noticed cardiovascular risk can also be associated with PCOS. VeryWellHealth makes it clear how this happens: 

“Having PCOS increases a woman’s chances of getting heart-related complications. 

This is due to the higher levels of insulin that have been associated with PCOS and are known to increase one’s risk for elevated triglycerides, low levels of high-density lipoprotein (HDL), high cholesterol, blood pressure, and atherosclerosis. These conditions can increase your risk for a heart attack and stroke.” 

I wonder if you’ve realized that CKD can also cause heart problems. The Kidney Fund clarifies: 

“The heart and the kidneys work closely together. When there is a problem with one, things can go wrong in the other. Heart disease can cause CKD, and CKD can also cause heart disease. 

When you have heart disease, your heart may not pump blood in the right way. Your heart may become too full of blood. This causes pressure to build in the main vein connected to your kidneys, which may lead to a blockage and a reduced supply of oxygen rich blood to the kidneys. This can lead to kidney disease. 

When the kidneys are not working well, your hormone system, which regulates blood pressure, has to work harder to increase blood supply to the kidneys. When this happens, your heart has to pump harder, which can lead to heart disease.”  

It is all connected. PCOS to diabetes to CKD to heart problems. Before you start to worry, it doesn’t have to be like that. Take care of yourself and prevent the diseases if you can. 

Until next week, 

Keep living your life! 

Never Heard of It Before

Before I get to what I’ve never heard of before, let’s pay homage to what I have heard of before. Therefore: Happy [yesterday] Father’s Day to all the fathers of all sexes and those acting as fathers. 

Photo by Cristian Dina on Pexels.com

While I’ve written about Juneteenth before, this is the first time I’m wishing you a glorious Juneteenth while it is a National Holiday. Good on you, Ms. Opal Lee! 

On to the kidney part of today’s blog. 

I’ve been a chronic kidney disease patient for 13 years and I have never, not even once, heard of Kremezin until another patient mentioned it. Not having a clue as to what it was, I turned to The National Center for Biotechnology Information (NCBI), a part of the United States National Library of Medicine (NLM), which is a branch of the National Institutes of Health (NIH). This is from a 2019 study published there: 

“AST-120 (KREMEZIN®) consists of oral, spherical carbon particles that adsorb uremic toxins and their precursors within the gastrointestinal tract, allowing them to be excreted in the feces. Uremic toxins such as indoxyl sulfate and p-cresyl sulfate are abundant in the blood of chronic kidney disease (CKD) patients and are related to the progression of both CKD and cardiovascular disease. AST-120 was approved in Japan in 1991 followed by Korea (2004), Taiwan (2007) and the Philippines (2010) for treating uremic symptoms and prolonging the time to initiation of dialysis in patients with progressive CKD.”   

As reported in BMC Nephrology last year:  

“OSCA effectively reduced serum IS levels in moderate to severe CKD patients. Gastrointestinal symptoms were the most commonly reported complications, but no treatment-related severe adverse effects were reported.” 

OSCA means oral spherical carbon adsorbent, a new kremezin type medication. According to their website: 

BMC Nephrology is an open access journal publishing original peer-reviewed research articles in all aspects of the prevention, diagnosis and management of kidney and associated disorders, as well as related molecular genetics, pathophysiology, and epidemiology.”   

Hmmm, it sounded like a pretty easy solution to slowing down the progression to dialysis and/or transplantation, so why didn’t I know about it? And why didn’t you? 

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Then I thought that it might have disastrous side effects and that’s why it wasn’t widely used in the United State. A 2010 Korean study in The Korean Journal of Nephrology disabused me of that idea: 

“The most common adverse effects of AST-120 were gastrointestinal symptom, such as constipation, abdominal discomfort, nausea/vomiting.” 

While not pleasant, [Those remind me very much of the side effects of chemotherapy.] you can live with these if you want to delay dialysis and/or transplantation. 

I was having trouble finding more information about carbon based medical products, so I thought I’d try a more generalized approach. Bingo! This is from a 2018  Henry Ford Health System’s Henry Ford Live Well Blog: 

“…. Many people are looking for ways to reduce inflammation and detox, so there’s a huge market for these products. The problem is, there’s no agency overseeing the safety or effectiveness of activated charcoal, and it’s not governed by the Food and Drug Administration (FDA). [I bolded that; it’s so important.] 

Breaking Down the Facts on Activated Charcoal 

Before you slip some activated charcoal in your morning protein shake, it’s important to note that activated charcoal is not the same as the charcoal you buy at Home Depot for your backyard barbeque, nor is it made from the same stuff as the char on your overdone toast. Instead, it comes from burning specific types of wood — including bamboo, birch and balsam — at super-high temperatures, then oxidizing it. 

The particles left behind are almost pure carbon, so they’re able to suck up moisture and chemicals. But that doesn’t mean using it is safe or should be done without medical supervision. 

Here are … facts you should know before you purchase anything with activated charcoal: 

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It draws out impurities. Charcoal has a rich history as a medical treatment. Its porous texture binds to toxins and prevents your body from absorbing them. That’s one reason it’s a staple in hospital emergency rooms. Doctors commonly use it as an antidote for food poisoning and drug toxicity…. 

It can bind to medications, vitamins and minerals. Activated charcoal does bind to chemical toxins to flush them out, but it also binds to nutrients. Take too much and you could compromise your nutrient status or interfere with the way your body absorbs medication. It can make blood pressure medication and even birth control pills less effective. 

It can help patients with kidney disease. For patients with end-stage renal disease, activated charcoal may be a viable alternative to dialysis. The reason: It binds to urea and other toxins, reducing the number of waste products that filter through your kidneys. If you have kidney disease, talk to your doctor…. [Again, my bolding.] 

The Bottom Line 

Activated charcoal is still a largely unstudied and misunderstood compound and as far as safety goes, consumers are at the mercy of the manufacturer. Any chemical that has the potential to do good also has the potential to harm. Only use activated charcoal under the direction of a medical professional, particularly if you’re planning to ingest it.”  

This is now hour three on today’s blog and I still haven’t found any evidence that Kremezin is FDA-approved or sold in the United States. It is clear that it is used in other countries and can be ordered from those countries. But I wouldn’t suggest it. I found prices ranging from $340.00 to $440.99 for 336 500 mg. tablets. That’s quite a discrepancy. Additionally, the granular form is still being sold even though it has harsher side effects. 

If you’re interested, speak with your nephrologist. There may be good reasons that I wasn’t able to unearth you shouldn’t take this drug, effective or not. Then again, there may be good reasons to take it. Precision Medicine dictates that we are all unique patients, and we are. What works for you may not work for me and vice-versa. But wow! What if you were introducing your nephrologist to a new drug to help slow down the progression of the decline of your kidney function? I sort of doubt that would be the case, but it just might be. 

Until next week, 

Keep living your life! 

It Gets a Little Confusing

I’m familiar with hospice, as I’m sure quite a few of us are.  Way back in 1988, they came to my folks’ house for my father when he had pancreatic cancer. When my mother could no longer physically take care of him, he was moved to a hospice facility. Although I lived in New York and they lived in Florida, I spent quite a bit of time in hospice with my father. I was terrified and wholly unaware of what this was or what they were doing for us. Thank goodness they were there to help us. 

The Hospice Foundation of America tells us what hospice is: 

“Medical care to help someone with a terminal illness live as well as possible for as long as possible, increasing quality of life. 

An interdisciplinary team of professionals who address physical, psychosocial, and spiritual distress focused on both the dying person and their entire family. 

Care that addresses symptom management, coordination of care, communication and decision making, clarification of goals of care, and quality of life.” 

When I had pancreatic cancer two years ago, it wasn’t hospice that I heard discussed, but palliative care. One problem, I didn’t know what it was. Get Palliative Care explains: 

“Palliative care is specialized medical care for people living with a serious illness. This type of care is focused on providing relief from the symptoms and stress of the illness. The goal is to improve quality of life for both the patient and the family. 

Palliative care is provided by a specially-trained team of doctors, nurses and other specialists who work together with a patient’s other doctors to provide an extra layer of support. Palliative care is based on the needs of the patient, not on the patient’s prognosis. It is appropriate at any age and at any stage in a serious illness, and it can be provided along with curative treatment.” 

Let’s take a look at these two different concepts. What’s the difference between them? Hospice is for those “with a terminal illness,” while palliative care is for those “with a serious illness.” Well, isn’t a serious illness terminal? 

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No, it isn’t. Some of you knew that already, but some of you didn’t. Terminal means end, like a train terminal… or the end of life. According to Johns Hopkins Medicine – in the medical sense – serious means: 

“Vital signs may be unstable and not within normal limits. Patient is acutely ill. Indicators are questionable.” 

Serious is not necessarily critical. Remember that the next time you call a hospital to ask about the condition of a friend or family member. 

I knew palliative care grew from the hospice movement, but I didn’t know how or why. I turned to UPMC (University of Pittsburgh Medical Center) Palliative and Supportive Institute for the answer: 

“…. Palliate comes from pallium, the Latin word for ‘cloak’. [The English teacher in me just had to include that information.] To palliate is to cloak, or cover up, the symptoms of an illness without curing it. This meaning grew into the idea of alleviating or reducing suffering.  

Palliative care got its start as hospice care, often delivered by caregivers at religious institutions. Dame Cicely Saunders, a British physician, founded the first formal hospice in 1948 specifically to care for patients with terminal illnesses. Her success in improving her patients’ quality of life led her to introduce the concept of hospice care to other physicians, who quickly recognized the value in respecting people’s wishes and needs at the end of life. Caregivers began to understand that these values could apply to patients without terminal illnesses as well.

A New Way of Caregiving

In 1990, the World Health Organization (WHO) recognized palliative care as a distinct specialty dedicated to relieving suffering and improving quality of life for patients with life-limiting illnesses or serious injuries. WHO described the goals of palliative care as the prevention, assessment, and multidisciplinary treatment of physical, spiritual, and psychological problems. Palliative care was now an established entity, separate from hospice and sometimes administered along with curative treatments, but hospitals were rather slow to adopt the practice.  

The Growth of Palliative Care 

Palliative care eventually began to catch hold in hospitals across the United States. Between 2000 and 2011, the prevalence of palliative care in U.S. hospitals with 50 or more beds has increased more than 157% (according to the Center to Advance Palliative Care). Today, palliative care programs ensure whole-person healthcare for patients in approximately 75% of all hospitals with more than 300 beds. As more people begin to understand and appreciate the benefits that palliative care offers, the specialty has become available in nursing homes, ambulatory care centers, and home care programs.” 

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Inpatient palliative care is widely accepted in the U.S. now, but what if you want palliative care at home? What can be done for you without entering the hospital?  

“Medical evaluations, including monitoring for common symptoms like nausea, vomiting, pain, and anxiety 

Prescribing medications to ease these symptoms 

Additional medical applications like treating wounds and other medical needs 

Physical therapy and other rehabilitation needs 

Providing emotional and spiritual support in addition to physical 

Providing social interaction 

Providing guidance on navigating the healthcare system and understanding individual healthcare needs” 

Thank you to Crosswords Hospice and Palliative Care for the above information. 

This is starting to sound a lot like home health care. I wondered if the two were the same. The Alliance had a wonderfully simple clarification and even included hospice: 

  • “Home health services help you get better from an illness or injury, regain your independence, and become as self-sufficient as possible. 
  • Palliative care is a form of home health care in which patients face chronic or quality of life-limiting illnesses, and focuses on the relief of symptoms, pain and stress. Patients may receive curative treatments. 
  • Hospice is for patients with a limited life expectancy, who are no longer receiving curative treatments for any terminal illness.” 

By the way, The Alliance is a pretty interesting group. This is how they describe themselves: 

“Employers are the second-largest purchaser of health care in the country, yet typically have little say in its price – which has gone up every year since 1996 – or its quality. However, by self-funding and banding together to leverage their purchasing power, employers can generate more control over their costs and demand better care for their dollar together.  

The Alliance serves as the voice of those self-funded employers who are tired of health care as usual; we’ve been creating clarity in health care for over 30 years by providing transparent, creative approaches to network and benefit plan design to unlock savings where others can’t – or won’t – using Smarter NetworksSM and sophisticated data mining and analysis.” 

What does any of this have to do with kidney disease? Palliative care is for kidney disease, too. 

Until next week, 

Keep living your life! 

A Point to Ponder 

It’s clear to me that it’s past time for me – and you – to understand this. When I first was diagnosed with Chronic Kidney Disease back in 2008, it was my understanding that Blacks, or Afro-Americans as they were referred to back then, had a higher muscle mass and that’s why there was a different algorithm for their GFR. But as Dr. Vanessa Grubbs has questioned, “This equation assumes that Black people are a homogeneous group of people, and doesn’t take into account, how Black is Black enough?” 

Before I forget [truly a valid concern these days], this is her profile from University of California, San Francisco’s Profiles

“Dr. Vanessa Grubbs is an Associate Professor in the Division of Nephrology at UCSF and has maintained a clinical practice and research program at Zuckerberg San Francisco General Hospital since 2009. Her research focuses on palliative care for patients with end-stage kidney disease. She is among the 2017 cohort for the Cambia Health Foundation Sojourns Scholar Leadership Program, an initiative designed to identify, cultivate and advance the next generation of palliative care leaders; and the 2018 California Health Care Foundation’s Health Care Leadership Program. 
 
Her clinical and research work fuel her passion for creative writing. Her first book, HUNDREDS OF INTERLACED FINGERS: A Kidney Doctor’s Search for the Perfect Match, was released June 2017 from Harper Collins Publishers, Amistad division and is now in paperback….”   

She has a valid point. We have children in the family who have a white mother and a Black father. Are they Black? They don’t look Black to me. Are they white? They don’t look white to me. Heaven forbid they were ever diagnosed with Chronic Kidney Disease, which GFR should be used? The one for Afro-Americans? The one for non-African Americans? And who decides? Their mother? Their father? Their future nephrologist? 

What about the children in the family who have a Mexican father and a white mother? Are they considered Black? They don’t look Black to me. Are they white? They don’t look white to me. Heaven forbid they were ever diagnosed with Chronic Kidney Disease, which GFR should be used? The one for Afro-Americans? The one for non-African Americans? And who decides? Their mother? Their father? Their future nephrologist? I repeated the same questions as for the previous children so you can see that we could go on with the same questions for just about every mother/father combination you can think of.  

As late as last month, Missouri State University’s Office for Institutional Equity and Compliance offers the following definitions: 

“African American – Nonwhite person of African descent who lives in the United States. Not a synonym for Black. See Black. 

Afro-American – Outdated synonym for African American. Although not a derogatory term, avoid when possible. Use Black or African American if appropriate. See African American, Black ….. 

Black – Nonwhite person of Black descent, regardless of national origin. Use Black only in this larger context. Use terms as African American, Haitian, etc. when race is known. See African American, white …. 

White – Defined by the U.S. Census Bureau as a person of descent from the original people of Europe, the Middle East and North Africa….” 

As far as I know Mexico is not in Europe, the Middle East, North Africa, or Africa. So where does this leave these kids and all other Mexico or biracial kids [and adults] when deciding which algorithm to use in calculating their GFR? Wait a minute, where does this leave all non-white, non-Black people? 

But what about muscle mass; how do you determine it before finding a GFR? Or do you?  

I was getting a bit confused here, so I turned to the National Kidney Foundation for help: 

“African American patients: The CKD-EPI and MDRD Study equations include a term for the African American race to account for the fact that African Americans have a higher GFR than Caucasians (and other races included in the CKD-EPI datasets and MDRD Study) at the same level of serum creatinine. This is due to higher average muscle mass and creatinine generation rate in African Americans …. 

Male and female patients: The CKD-EPI and MDRD Study equations include a term for female sex to account for the fact that men have a higher GFR than women at the same level of serum creatinine. This is due to higher average muscle mass and creatinine generation rate in men…. 

Age: The CKD-EPI and MDRD Study equations include a term for age to account for the fact that younger people have a higher GFR than older people at the same level of serum creatinine. This is due to higher average muscle mass and creatinine generation rate in younger people …..” 

So, it’s not just Blacks’ GFRs that are calculated differently due to muscle mass. It’s also men of any race and younger people. I am not a doctor but then it doesn’t make any sense to me that there are two result categories: African American and non-African American. Why not Average Muscle Mass and Higher Muscle Mass? 

I neglected to explain what CKD-EPI and MDRD are: 

“In adults, the most widely-used equations for estimating glomerular filtration rate (GFR) from serum creatinine are the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation … and the isotope dilution mass spectrometry (IDMS) traceable Modification of Diet in Renal Disease (MDRD) Study equation ….” 

Thank you to The National Institutes of Health’s National Institute of Diabetes, Digestive, and Kidney Diseases for that explanation. I’ve got to admit that all I got was that these two equations are used to estimate the GFR or Glomerular Filtration Rate. It’s the GFR that determines if you have CKD and, if you do, what stage you’re in.  

Somehow, I feel there’s more to this, especially since the National Kidney Foundation in conjunction with the American Society of Nephrology has created a task force exploring the possibilities for excluding race in the GFR algorithm. Stay tuned. 

Until next week, 

Keep living your life! 

To Biopsy or Not to Biopsy

My husband of eight years, Bear, is a veteran. We won’t be celebrating him today, but we will on Veterans Day. Today, we celebrate those who weren’t able to return to us, to marry, to have children or grandchildren, to further their education, or start the business of their dreams. Today, we celebrate those who never got the chance to discover and develop their art or their craft, the ones who didn’t grow older. Today is Memorial Day and we remember all those who fought so we didn’t have to. I’ve thrown in a couple of clichés because they work here; they’re meaningful. Thank you fallen warriors for your sacrifice and thank you to your families, too. 

There is no way to glide into today’s blog topic from the above tribute, so I’ll just plunge ahead. 

I read about people having kidney biopsies all the time and I wonder why I never had one. Mind you, I’ve been wondering this for well over a decade. It’s time to find out, don’t you think? 

For those who don’t recognize the term: 

“A biopsy is a procedure that removes cells or tissue from your body. A doctor called a pathologist looks at the cells or tissue under a microscope to check for damage or disease. The pathologist may also do other tests on it. 

Biopsies can be done on all parts of the body. In most cases, a biopsy is the only test that can tell for sure if a suspicious area is cancer. But biopsies are performed for many other reasons too. 

There are different types of biopsies. A needle biopsy removes tissue with a needle passed through your skin to the site of the problem. Other kinds of biopsies may require surgery.” 

Thank you to MedlinePlus for that information. MedlinePlus is part of the U.S. National Library of Medicine which, in turn, is part of the National Institutes of Health. 

Oh, a little more about pathologists. They study the causes and effects of diseases, so it makes sense that they would be the ones at the microscope.  

Let me give you an example of a biopsy. We all know I had pancreatic cancer. It was diagnosed via a fine needle aspiration. WebMD explains: 

“In fine needle aspiration, a thin needle is inserted into an area of abnormal-appearing tissue or body fluid. As with other types of biopsies, the sample collected during fine needle aspiration can help make a diagnosis or rule out conditions such as cancer. Fine needle aspiration is generally considered a safe procedure. Complications are infrequent.” 

Because the organ being biopsied was the pancreas, a needle could not be inserted into the skin. The pancreas is well hidden in the body, so an endoscopy was performed. That’s the opposite of a colonoscopy. [Lots of ‘scope’ or ‘scopy’ words today.] Instead of a long thin tube being inserted into the anus, it was inserted into the mouth and a fine needle was threaded through this tube to obtain the necessary tissue. 

Got it? Now, how is a kidney biopsy performed and why? Or in my case, why not? 

I turned to my trusted friend The MayoClinic for some answers. 

“A kidney biopsy may be done to: 

Diagnose a kidney problem that can’t otherwise be identified 

Help develop treatment plans based on the kidney’s condition 

Determine how quickly kidney disease is progressing 

Determine the extent of damage from kidney disease or another disease 

Evaluate how well treatment for kidney disease is working 

Monitor the health of a transplanted kidney or find out why a transplanted kidney isn’t working properly”  

Well, that all makes sense to me so why didn’t my nephrologist order one for me? [I’m starting to sound like the one kid in the class who wasn’t invited to the birthday party.] The paper Patient education: Kidney (renal) biopsy (Beyond the Basics) written by William L Whittier, MD, FASN and Stephen M Korbet, MD, MACP published on UpToDate clarified for me: 

“The following are the most common reasons for kidney biopsy. You may have one or more of these problems, but not everyone with these problems needs a kidney biopsy: 

●Blood in the urine (called hematuria). … 

●Protein in the urine (called proteinuria) – This occurs in many people with kidney problems. A kidney biopsy may be recommended if you have high or increasing levels of protein in the urine or if you have proteinuria along with other signs of kidney disease…. 

●Problems with kidney function – If your kidneys suddenly or slowly stop functioning normally, a kidney biopsy may be recommended, especially if the cause of your kidney problem is unclear.” 

Oh, I see. I didn’t have hematuria and my proteinuria was minimal. The cause of the problem seemed to be clear. I was getting older and so were my kidneys. [Maybe I really didn’t want to be invited to this birthday party after all.] 

I still wanted to know how the procedure was done. Was a needle really stuck through your skin? Did it hurt? The National Institute of Diabetes, and Digestive and Kidney Diseases, also part of the National Institutes of Health, offered an extremely detailed answer. 

“The procedure typically takes about an hour and includes the following steps: 

Most people will lie on their abdomen on an examination table. The technician will place a firm pillow or sandbag under a person’s body to support the abdomen and help push the kidneys up toward the person’s back and the surface of the skin. People who have a transplanted kidney lie on their backs because surgeons place transplanted kidneys in the front-lower part of the abdomen, to one side of the bladder. 

A nurse or technician will give the person sedatives through the IV. 

The health care provider will mark the point where the needle will enter the skin, clean the area, and inject a local anesthetic to numb the area. 

Next, the health care provider uses imaging techniques, such as ultrasound, to guide the biopsy needle into the kidney. Ultrasound uses a device called a transducer that bounces safe, painless sound waves off organs to create an image of their structure. Sometimes the health care provider uses a computerized tomography scan or magnetic resonance imaging to guide the needle into the kidney. 

The health care provider will ask the person to hold his or her breath and stay still as the health care provider inserts the biopsy needle and removes the kidney tissue. When the health care provider takes the biopsy, the instrument will make a clicking or popping noise. The health care provider may need to insert the needle three or four times. People most often will need to hold their breath for about 30 seconds or a little longer for each insertion. 

The health care provider uses imaging techniques such as ultrasound to guide the biopsy needle into the kidney. 

For people with bleeding problems, the health care provider uses a laparoscope—a thin tube with a video camera. This procedure is surgery that requires general anesthesia. The surgeon makes a small incision into the back and inserts the laparoscope to see the kidney. The surgeon can insert tiny tools through the laparoscope to collect tissue samples and can watch after the procedure through the camera to make sure that if there is any bleeding, he or she can stop it.” 

Now I know… and so do you. 

Until next week, 

Keep living your life! 

A Question I Never Did Answer

 This has been a week fraught with the good (my friend’s high school graduation) and the bad (settling someone’s estate). I didn’t realize until yesterday that today would be Monday. What was I going to write about? I hadn’t really thought about it. Oh wait. Somewhere along the line recently, someone or some company asked me about Losartan. Good question. I could write about that.  I guess I’d better get digging. 

First thing I did was check Drugs.com to see what it is. 

“Losartan (Cozaar) belongs to a group of drugs called angiotensin II receptor antagonists. [Gail here: also called an ARB.] It keeps blood vessels from narrowing, which lowers blood pressure and improves blood flow. 

Losartan is used to treat high blood pressure (hypertension). It is also used to lower the risk of stroke in certain people with heart disease. 

Losartan is used to slow long-term kidney damage in people with type 2 diabetes who also have high blood pressure. 

Losartan may also be used for purposes not listed in this medication guide.” 

Now I know why it was mentioned to me. I have both high blood pressure and type 2 diabetes. But I’m not so sure I understand how it works. 

Let’s start figuring it out by defining angiotensin II receptor antagonists. First, we need to know that angiotensin ll receptor antagonists and angiotensin ll receptor blockers are one and the same. Now, Mayo Clinic to the rescue: 

“Angiotensin II receptor blockers help relax your veins and arteries to lower your blood pressure and make it easier for your heart to pump blood. 

Angiotensin is a chemical in your body that narrows your blood vessels. This narrowing can increase your blood pressure and force your heart to work harder. 

Angiotensin II receptor blockers block the action of angiotensin II. As a result, the medication allows your veins and arteries to widen (dilate).” 

Wait a minute here. If angiotensin is the chemical, why is there an ‘II’ after that word in the name of the receptor blocker? [I really do wonder about things like this.] Are you ready for this? According to  Encyclopaedia Britannica, there are not one, not two, but three kinds of angiotensin: 

“There are three forms of angiotensin. Angiotensin I is produced by the action of renin (an enzyme produced by the kidneys) on a protein called angiotensinogen, which is formed by the liver. Angiotensin I is transformed into angiotensin II in the blood by the action of angiotensin-converting enzyme (ACE). Angiotensin II acts directly on blood vessels, causing their constriction and thereby raising blood pressure. This substance also can cause vessel constriction through indirect mechanisms, such as by stimulating the release of the steroid hormone aldosterone and substances called catecholamines from the adrenal glands and by blocking the reuptake of the hormone norepinephrine into neurons. Angiotensin III is a metabolite of angiotensin II and shares similar, though less potent, actions.” 

Look at that kidney involvement, will you. But we are going down the rabbit hole, aren’t we? Okay, let’s get to it. The logical next step is to define aldosterone.  You and Your Hormones does just that: 

“Aldosterone is a steroid hormone. Its main role is to regulate salt and water in the body, thus having an effect on blood pressure.” 

Salt and water, also important to kidney function. 

So, what are catecholamines and why are they important to those of us with kidney disease? 

“Catecholamines increase heart rate, blood pressure, breathing rate, muscle strength, and mental alertness. They also lower the amount of blood going to the skin and intestines and increase blood going to the major organs, such as the brain, heart, and kidneys.” 

Thank you to the University of Michigan’s Michigan Medicine for an explanation that is easily understood. Did you notice the kidney involvement here, too? 

Just one more definition, but you need to know that norepinephrine and noradrenaline are the same thing. [Confusing!] I turned to Lumen Boundless Biology for help: 

“Norepinephrine, produced by the adrenal medulla, is a stress hormone that increases blood pressure, heart rate, and glucose from energy stores; in the kidneys, it will cause constriction of the smooth muscles, resulting in decreased or inhibited flow to the nephrons.” 

Uh-huh, the kidneys again. 

Alright, so it all sounds good to go with Losartan in that it will be helpful for your kidneys. Aha! That is not exactly the case. It turns out that doctors do not start kidney disease patients at the highest doses of losartan since that may cause hyperkalemia, better known as high potassium. Here’s a conundrum: Losartan can also cause kidney disease. This is what MedicalNewsToday tells us are the possible serious side effects of taking losartan. 

“High potassium blood levels. Symptoms can include: 

heart rhythm problems 

muscle weakness 

slow heart rate 

Allergic reactions. Symptoms can include: 

swelling of your face, lips, throat, or tongue 

Low blood pressure. Symptoms can include: 

feeling faint or dizzy 

Kidney disease. Symptoms can include: 

swelling in your feet, ankles, or hands 

Unexplained weight gain” 

Does this mean don’t take losartan even if it’s prescribed by your family doctor or nephrologist? No, not at all. It simply means you have to be carefully monitored. Remember, I’m not a doctor nor have I ever claimed to be one, so I urge you to check with yours. 

I kept running across RAAS in my searching. It turns out that mean Renin-Angiotensin- Aldosterone System. What’s that? Beats me. But the Merck Manual, Consumer Version knows: 

“Regulating Blood Pressure: The Renin-Angiotensin-Aldosterone System 

The renin-angiotensin-aldosterone system is a series of reactions designed to help regulate blood pressure. 

When blood pressure falls (for systolic, to 100 mm Hg or lower), the kidneys release the enzyme renin into the bloodstream. 

Regulating Blood Pressure: The Renin-Angiotensin-Aldosterone System

Renin splits angiotensinogen, a large protein that circulates in the bloodstream, into pieces. One piece is angiotensin I. 

Angiotensin I, which is relatively inactive, is split into pieces by angiotensin-converting enzyme (ACE). One piece is angiotensin II, a hormone, which is very active. 

Angiotensin II causes the muscular walls of small arteries (arterioles) to constrict, increasing blood pressure. Angiotensin II also triggers the release of the hormone aldosterone from the adrenal glands and vasopressin (antidiuretic hormone) from the pituitary gland. 

Aldosterone and vasopressin cause the kidneys to retain sodium (salt). Aldosterone also causes the kidneys to excrete potassium. The increased sodium causes water to be retained, thus increasing blood volume and blood pressure.” 

And it all comes full circle. Oh, one last thing: too much activation of the RAAS causes kidney disease. Oh, my. 

Until next week, 

Keep living your life! 

I’ve Had Cancer, But Not This Kind

Several days ago, I received a call from a cousin who I haven’t seen nor heard from since my brother’s funeral almost three years ago. You know that can’t be good… and it wasn’t. It seems she might have kidney cancer. We are a cancer prone family, but this is the first possible diagnose of this kind. She wanted to know what I knew about it and I had nothing to tell her. But I will after this blog and you’ll know a lot more about it, too.  

Having no knowledge of this kind of cancer except that it starts in the kidneys, I decided my usual go-to the Mayo Clinic might be the best place for a general overview. 

“In adults, renal cell carcinoma is the most common type of kidney cancer. Other less common types of kidney cancer can occur. Young children are more likely to develop a kind of kidney cancer called Wilms’ tumor. 

The incidence of kidney cancer seems to be increasing. One reason for this may be the fact that imaging techniques such as computerized tomography (CT) scans are being used more often. These tests may lead to the accidental discovery of more kidney cancers. Kidney cancer is often discovered at an early stage, when the cancer is small and confined to the kidney.” 

Let’s not forget that the kidneys are buried deep in the body where a physical examination may not reach for signs of tumors. 

My cousin said she had no symptoms. Was that usual with this type of cancer? I know from my own experience that sometimes those with Chronic Kidney Disease have no symptoms, but this was cancer. The Cancer Treatment Centers of America laid out the possible symptoms for us: 

“The most common sign of kidney cancer is blood in the urine (hematuria), which may make the urine look rusty or dark red. Other signs of kidney cancer may include:  

Low back pain or pressure on one side that doesn’t go away 

A mass or lump on the side or lower back 

Fatigue 

Loss of appetite or unexplained weight loss 

A persistent fever not caused by infection 

Anemia (low red blood cell count) 

Swelling of the ankles and legs 

In men, a cluster of enlarged veins, called a varicocele, around a testicle, typically, the right testicle 

Although these symptoms may indicate a kidney tumor, they also may be caused by other, less serious health issues. Some kidney cancer patients experience none of these signs, and others experience different symptoms entirely.” 

I was curious as to how my cousin knew what her primary physician suspected since she’d told me she hadn’t had a biopsy yet. WebMD explained the other tests she may have undergone. 

“Urine tests check for blood in your urine or other signs of problems. 

Blood tests show how well your kidneys are working. 

Intravenous pyelogram (IVP) involves X-raying your kidneys after the doctor injects a dye that travels to your urinary tract, highlighting any tumors. 

Ultrasound uses sound waves to create a picture of your kidneys. It can help tell if a tumor is solid or fluid-filled. 

A CT scan uses X-rays and a computer to create a series of detailed pictures of your kidneys. This may also require an injection of dye. CT scans have virtually replaced pyelogram and ultrasound as a tool for diagnosing kidney cancer. 

Magnetic resonance imaging (MRI) uses strong magnets and radio waves to create detailed images of soft tissues in your body. You may need an injection of a contrast agent to create better pictures. 

Renal arteriogram. This test is used to evaluate the blood supply to the tumor. It is not given often but may help diagnose small tumors. It has other uses, as well.” 

While blood and urine tests can also confirm CKD and are familiar to us, renal arteriogram was something that was new to me. So, it sounds like she may go straight to CT since both the pyelogram and ultrasound are not as effective in diagnosing kidney cancer. 

Picture this. My cousin has been diagnosed and is going slightly berserk. Cancer is not an easy diagnosis. She goes to her primary doctor and (s)he refers her to one of these specialists who will bring in the rest of the team: 

“In cancer care, different types of doctors often work together to create a patient’s overall treatment plan that combines different types of treatments. This is called a multidisciplinary team. For kidney cancer, the health care team usually includes these individuals: 

Urologist. A doctor who specializes in the genitourinary tract, which includes the kidneys, bladder, genitals, prostate, and testicles. 

Urologic oncologist. A urologist who specializes in treating cancers of the urinary tract. 

Medical oncologist. A doctor trained to treat cancer with systemic treatments using medications. 

Radiation oncologist. A doctor trained to treat cancer with radiation therapy. This doctor will be part of the team if radiation therapy is recommended. 

Cancer care teams include a variety of other health care professionals, such as physician assistants, nurse practitioners, oncology nurses, social workers, pharmacists, counselors, dietitians, and others.” 

Cancer.net, which is doctor approved patient information from the American Society of Clinical Oncologists, was my source for this information. 

Wait a minute. “What’s the role of the nephrologist in all this? After all, that’s the kidney specialist,” my cousin may ask. According to UCLA Health’s Core-Kidney

“Nephrologists screen and identify kidney cancer patients that are at high risk of developing CKD after surgery. Nephrologists team with urologists for ‘before and after surgery’ care of patients. Nephrologists are routinely consulted for optimization of blood pressure of kidney cancer patients, correction of anemia, avoidance of drugs that are potentially toxic to kidneys and adequate hydration of kidneys during contrast use with computer tomography or during surgery.” 

I know, I know. What’s important to her right now is how this kidney cancer may be treated. I went straight to the horse’s mouth (so to speak) for help with this one. The National Kidney Foundation offers a multitude of options. To paraphrase, they are: 

Open, laparoscopic surgery, or robotic surgery to remove part or all of the kidney 

Thermal ablation 

Active Surveillance 

Chemotherapy and Radiation 

There are more options for advanced kidney cancer. 

For the first time in a decade, I don’t know how to end this blog. Let’s put it this way; I’ve had cancer, even though it wasn’t kidney cancer and I just plain hope cancer is not something you’ll have to deal with. 

Until next week, 

Keep living your life! 

How Do You Know? 

Often, people will ask me how I knew I had Chronic Kidney Disease. I didn’t have any symptoms although I did suffer from high blood pressure, which is the second most common cause of CKD. Well, how did I know then?

When I changed doctors to one closer to my home, she had her own set of thorough tests completed for me as a new patient. One of them was the eGFR [estimated Glomerular Filtration Rate]. She saw that 39% and had me in a nephrologist’s office the next day. The National Kidney Foundation explains why:  

“When your kidneys are working well, they filter out wastes and excess fluid that become part of the urine your body makes each day. When kidneys aren’t working well, you do not remove enough wastes and fluids to keep you healthy. You also cannot make important hormones for your blood and bones. Your GFR number is an estimate of how well your kidneys are working and keeping you healthy. If your GFR number is low, your kidneys are not working as well as they should. Early detection will allow for early treatment. Early treatment may keep kidney disease from getting worse.” 

Remember those old television commercials that announced, “But wait! There’s more.” That applies here, too. In addition to the blood test for eGFR, I needed a urine test. Thank you to The American Kidney Fund for revealing the necessity of this: 

“When your kidneys are damaged, they may let protein leak into your urine. This can be one of the earliest signs of kidney disease. To check for protein in your urine (called proteinuria), your doctor may suggest a urine test. There are two types of urine tests your doctor may use. 

Dipstick urine test 

A dipstick urine test tells your doctor if there is protein in your urine. Your doctor may test your urine in the office or ask you to bring a sample from home. If your first dipstick urine test shows protein in your urine, ask your doctor when you should be tested again. Also ask if a urine albumin-to-creatinine (UACR) test is right for you. 

Urine albumin-to-creatinine ratio (UACR) 

A UACR test tells your doctor how much albumin is in your urine. Your doctor will test your urine to see how much albumin (a type of protein) and creatinine (a kind of waste) are in it. Your doctor will compare these results to figure out your UACR. A normal UACR is less than 30mg/g. If your UACR is more than 30 mg/g, ask your doctor when you should be tested again. Also ask your doctor if you should have an eGFR test.” 

These two tests, the former gold standard for assessing CKD, seem to be falling out of favor. You see, the blood test relies on race as one of its elements. I was taught that was because Afro-Americans have a denser muscle mass. Okay, that seemed acceptable. It also seems that this is no longer acceptable. I understand that racism must be combatted, but what about the science of denser muscle mass? If I’m correct, that’s one of the reasons Cystatin-C is slowly becoming the norm in CKD testing, but certainly not the only one.  

What is Cystatin-C? Let’s find out together. The most easily understood explanation I found was. The Medical Center of the University of Rochester’s

“Your body makes cystatin C constantly, and the protein is found in different fluids, including blood, spinal fluid, and breast milk. When your kidneys are healthy, they filter cystatin C out of the blood so it can be excreted in your urine. 

This is a fairly sensitive blood test to look at your kidney health. Cystatin C can be used to calculate your glomerular filtration rate (GFR). Your healthcare provider can use this to see how well your kidneys are working and if there is a problem. It can also be used to check the progress of your disease, if you have kidney problems.” 

I wasn’t sure enough about this being the best test for CKD, so I turned to Lab Tests Online to see what they had to say. 

“Because cystatin C levels fluctuate with changes in GFR, there has been interest in the cystatin C test as one method of evaluating kidney function. Tests currently used include creatinine, a byproduct of muscle metabolism that is measured in the blood and urine, blood urea nitrogen (BUN), and eGFR (an estimate of the GFR usually calculated from the blood creatinine level). Unlike creatinine, cystatin C is not significantly affected by muscle mass (hence, sex or age), race, or diet, which has led to the idea that it could be a more reliable marker of kidney function and potentially used to generate a more precise estimate of GFR. 

While there are growing data and literature supporting the use of cystatin C, there is still a degree of uncertainty about when and how it should be used. However, testing is becoming increasingly more available and steps are being taken toward standardizing the calibration of cystatin C results.” 

Ah, I see, race need not be taken into account. Hmmm, neither does sex, age, or diet. This almost sounds too good to be true. 

Whoops! I haven’t reminded you what the BUN [blood urea nitrogen] test mentioned above is. My longtime standby, The Mayo Clinic clarifies: 

“A common blood test, the blood urea nitrogen (BUN) test reveals important information about how well your kidneys and liver are working. A BUN test measures the amount of urea nitrogen that’s in your blood. 

Here’s how your body typically forms and gets rid of urea nitrogen: 

Your liver produces ammonia — which contains nitrogen — after it breaks down proteins used by your body’s cells. 

The nitrogen combines with other elements, such as carbon, hydrogen and oxygen, to form urea, which is a chemical waste product. 

The urea travels from your liver to your kidneys through your bloodstream. 

Healthy kidneys filter urea and remove other waste products from your blood. 

The filtered waste products leave your body through urine. 

A BUN test can reveal whether your urea nitrogen levels are higher than normal, suggesting that your kidneys or liver may not be working properly.” 

Considering the information uncovered in today’s blog, I don’t think I’d mind at all if my nephrologist started to use the Cystatin-C method to test my eGFR. How about you? 

Until next week, 

Keep living your life! 

What About My Kids?

It’s May already. I don’t know if it’s lockdown that’s making the months seem to fly by or if it’s that I don’t look at the calendar very often. Either way, I know my first born’s birthday is May 6th. Happy birthday, my lovely Nima. By the way, Nima is Tibetan for the sun and my world did revolve around her just as our planet revolves around the sun. 

But when I was diagnosed with Chronic Kidney Disease way back in 2008, I became a bit nervous. Was this something I could conceivably [nice play on words, huh?] have passed on to her or her younger sister… and now that sister’s son? You’ve probably figured out that this mother worried about her children became the world’s best researcher overnight. Hmmm, that was 13 years ago. I wonder what the current research tells us about this. 

According to the University of Michigan’s Michigan Medicine, over 60 types of kidney disease can be inherited. These include: 

“Autosomal Dominant Polycystic Kidney Disease (ADPKD): The most common inherited kidney illness, ADPKD causes cysts to form on the kidneys. It occurs in about one in 800 people, and is passed down from parent to child through generations. Major health problems from ADPKD usually occur in adulthood, with more than 30,000 people in the U.S. each year suffering kidney failure as a result.  

Autosomal Recessive Polycystic Kidney Disease (ARPKD): This condition is also characterized by cysts, and affects about 1 in 20,000 people. ARPKD generally causes symptoms in early to late childhood. Learn more about dominant and recessive polycystic kidney disease on the PKD Foundation website. 

Thin Basement Membrane Disease 

Gitelman and Bartter Syndromes 

Collagen-related kidney diseases including Alport Syndrome: Learn more about Alport Syndrome on the Alport Syndrome Foundation website.  

Lowe Syndrome: Learn more about Lowe Syndrome on the Lowe Syndrome Association website. 

Hereditary Interstitial Kidney Disease: Gout associated inherited kidney diseases 

Tuberous Sclerosis 

Cystinosis: Learn more about Cystinosis on the Cystinosis Research Network website. 

Fabry Disease 

Nephronophthisis” 

While I’ve written about many of these, there are some that are new to me – and possibly to you – so I’ll write just a little bit about each of those. Also note that some of the websites are linked for you. 

Thank you, UNC School of Medicine‘s Kidney Center for the following: 

“TBM disease (also known as benign familial hematuria and thin basement membrane nephropathy) is, along with IgA nephropathy, the most common cause of blood in the urine without any other symptoms. The only abnormal finding in this disease is a thinning of the basement membrane of the glomeruli (filters) in the kidneys. Most patients with TBM disease maintain normal kidney function throughout their lives.” 

I haven’t written about Gitelman Syndrome. Luckily, there’s NORD to help us out here: 

“Fundamentally, like Bartter’s syndrome, Gitelman syndrome is a salt wasting nephropathy. The symptoms and severity of the disorder can vary greatly from one person to another and can range from mild to severe. For unknown reasons, the onset of symptoms is frequently delayed until the second decade of life. Symptoms and severity can even vary among members of the same family. Common symptoms can include episodes of fatigue, muscle weakness, and muscle cramps sometimes accompanied by gastrointestinal problems such as abdominal pain, nausea and vomiting. Some individuals may need to urinate frequently and will pass a large volume of urine (polyuria).” 

I turned to an old reliable favorite, MedlinePlus for information about Lowe Syndrome: 

“Kidney (renal) abnormalities, most commonly a condition known as renal Fanconi syndrome, often develop in individuals with Lowe syndrome. The kidneys play an essential role in maintaining the right amounts of minerals, salts, water, and other substances in the body. In individuals with renal Fanconi syndrome, the kidneys are unable to reabsorb important nutrients into the bloodstream. Instead, the nutrients are excreted in the urine. These kidney problems lead to increased urination, dehydration, and abnormally acidic blood (metabolic acidosis). A loss of salts and nutrients may also impair growth and result in soft, bowed bones (hypophosphatemic rickets), especially in the legs. Progressive kidney problems in older children and adults with Lowe syndrome can lead to life-threatening renal failure and end-stage renal disease (ESRD).” 

Cystinosis sounded somewhat familiar, but then I thought perhaps it was because it starts with “cyst.” It turns out I was wrong, as the Cystinosis Foundation explains: 

“Cystinosis is the most common inherited cause of Fanconi syndrome, a renal tubular disease characterized by the inability of the kidneys to reabsorb electrolytes, amino acids, proteins and glucose from the urine. This leads to the loss of large volumes of urine, salts, minerals and nutrients. Laboratory testing may reveal severe electrolyte abnormalities, including low potassium (hypokalemia), low phosphorus (hypophosphatemia) and low bicarbonate (metabolic acidosis). Fanconi syndrome leads to growth failure, excessive thirst (polydipsia), excessive urination (polyuria), and soft bones (rickets). Treatment of Fanconi syndrome requires replacing lost electrolytes such as potassium, phosphorus and bicarbonate. 

Without treatment, children with cystinosis progress to end-stage kidney failure by an average age of 8-10 years. Even with treatment, many children develop kidney failure in adolescence. In the past, this meant death. Today patients can be treated with dialysis and kidney transplantation. Even with a transplant, however, the disease continues to affect every other organ in the body.” 

I think we have room for one more, so let’s look at Nephronophthisis. A site that is new to me, The Weizmann Institute of Science’s Malacards, explained succinctly: 

“It is characterized by inflammation and scarring (fibrosis) that impairs kidney function. These abnormalities lead to increased urine production (polyuria), excessive thirst (polydipsia), general weakness, and extreme tiredness (fatigue). In addition, affected individuals develop fluid-filled cysts in the kidneys, usually in an area known as the corticomedullary region. Another feature of nephronophthisis is a shortage of red blood cells, a condition known as anemia. Nephronophthisis eventually leads to end-stage renal disease (ESRD), a life-threatening failure of kidney function that occurs when the kidneys are no longer able to filter fluids and waste products from the body effectively. Nephronophthisis can be classified by the approximate age at which ESRD begins: around age 1 (infantile), around age 13 (juvenile), and around age 19 (adolescent).” 

I got so involved with these diseases, that I almost forgot about CKD. It turns out that it may run in families, just as hypertension and diabetes may. While hypertension runs in my family, diabetes runs in my children’s father’s family. That means, I’m sorry to say, that they are at considerable risk of CKD since hypertension and diabetes are the two main causes of CKD. Nuts! 

Until next week, 

Keep living your life! 

How Is It Done?

A slightly belated welcome to the last week of National Donate Life Month to you. I have learned so much about kidney donation via my research for the blog this month, and hope you have, too. What makes more sense than to take a look at the donation process this week? 

Ready? I suppose the physical donation is the first part of the process so let’s look at that first. This is what Jefferson Heath, the home of Home of Sidney Kimmel Medical College, had to say about deceased donors: 

“It isn’t necessary to match the donor and recipient for age, sex or race. All donors are screened for hepatitis viruses and the HIV virus. What’s more, all deceased donor organs are tested extensively to help ensure that they don’t pose a health threat to the recipient. Also, many studies – such as ABO blood type and HLA matching – are performed to ensure that the organs are functioning properly. 

As soon as a deceased donor is declared brain-dead, the kidneys are removed and placed in sterile fluid similar to fluid in body cells. They are then stored in the refrigerator. The harvested kidneys need to be transplanted within 24 hours of recovery – which is why recipients are often called to the hospital in the middle of the night or at short notice.” 

I wondered if the process were different for a living donation. The Mayo Clinic tells us: 

“Both you and your living kidney donor will be evaluated to determine if the donor’s organ is a good match for you. In general, your blood and tissue types need to be compatible with the donor. 

However, even if your donor isn’t a match, in some cases a successful transplant may still be possible with additional medical treatment before and after transplant to desensitize your immune system and reduce the risk of rejection.” 

Now to the actual process. Johns Hopkins offered this very clear explanation of the process: 

“Generally, a kidney transplant follows this process: 

You will remove your clothing and put on a hospital gown. 

An intravenous (IV) line will be started in your arm or hand. More catheters may be put in your neck and wrist to monitor the status of your heart and blood pressure, and to take blood samples. Other sites for catheters include under the collarbone area and the groin blood vessels. 

If there is too much hair at the surgical site, it may be shaved off. 

A urinary catheter will be inserted into your bladder. 

You will be positioned on the operating table, lying on your back. 

Kidney transplant surgery will be done while you are asleep under general anesthesia. A tube will be inserted through your mouth into your lungs. The tube will be attached to a ventilator that will breathe for you during the procedure. 

The anesthesiologist will closely watch your heart rate, blood pressure, breathing, and blood oxygen level during the surgery. 

The skin over the surgical site will be cleansed with an antiseptic solution. 

The healthcare provider will make a long incision into the lower abdomen on one side. The healthcare provider will visually inspect the donor kidney before implanting it. 

The donor kidney will be placed into the belly. A left donor kidney will be implanted on your right side; a right donor kidney will be implanted on your left side. This allows the ureter to be accessed easily for connection to your bladder. 

The renal artery and vein of the donor kidney will be sewn to the external iliac artery and vein. 

After the artery and vein are attached, the blood flow through these vessels will be checked for bleeding at the suture lines. 

The donor ureter (the tube that drains urine from the kidney) will be connected to your bladder. 

The incision will be closed with stitches or surgical staples. 

A drain may be placed in the incision site to reduce swelling. 

A sterile bandage or dressing will be applied.” 

I wanted to know if there might be side effects or something else I should worry about as a kidney transplant recipient. The United Kingdom’s National Health Service was detailed in their response: 

Short-term complications 

Infection 

Blood clots 

Narrowing of an artery 

Arterial stenosis can cause a rise in blood pressure.  

Blocked ureter 

Urine leakage 

Acute rejection 

Long-term complications 

Immunosuppressant side effects: 

an increased risk of infections 

an increased risk of diabetes 

high blood pressure 

weight gain 

abdominal pain 

diarrhoea 

extra hair growth or hair loss 

swollen gums 

bruising or bleeding more easily 

thinning of the bones 

acne 

mood swings 

an increased risk of certain types of cancer, particularly skin cancer” 

Not everyone experiences these complications, nor are they insurmountable as far as I can tell. 

But what about the donor? Could he experience any ill effects? According to the trusted and respected National Kidney Foundation

“You will also have a scar from the donor operation- the size and location of the scar will depend on the type of operation you have. 

Some donors have reported long-term problems with pain, nerve damage, hernia or intestinal obstruction. These risks seem to be rare, but there are currently no national statistics on the frequency of these problems. 

In addition, people with one kidney may be at a greater risk of: 

high blood pressure 

Proteinuria 

Reduced kidney function” 

Naturally, as a donor, you’ll also be concerned about the financial aspects of donating. UNOS has information about this: 

Medical bills 

The transplant patients’ health insurance, Medicaid, or Medicare may cover these costs: 

Testing 

Surgery 

Hospital stay 

Follow-up care related to donation 

Personal bills 

Paid vacation and sick leave… 

Tax deductions and credits… 

Time off… 

Tax deductions or credits for travel costs and time away from work… 

Short-term disability insurance… 

FMLA (Family and Medical Leave Act) … 

NLDAC (National Living Donor Assistance Center) … 

AST (American Society of Transplantation) … 

Other 

Your private insurance or a charity may also cover costs you get during donation related to: 

Travel 

Housing 

Childcare” 

Not everyone is entitled to these financial aids. It depends on your employer, your length of time at that job, your state, and previous financial standing. 

You’ve probably noticed how little Gail there is in today’s blog and how much research there is. Remember, I knew extraordinarily little about transplant before writing this month’s blogs. 

Until next week, 

Keep living your life! 

And Then There’s Living Donation

This week just flew by. I guess good news does that. The good news is that this blog is live on Spotify. Just download the free app and enter SlowItDownCKD in the search bar. There we are. Most of the blogs take about seven and a half minutes of listening time. We’re also live on Anchor, Google Podcasts, Pocket Casts, RadioPublic, and Copy RSS. The link is https://anchor.fm/slowitdownckd. Of course, the digital and print books are still available on Amazon.  

Sometimes, kidney transplants are live, too. [How do you like that easy transition to today’s topic?] What do I mean, exactly? I mean the kidney to be transplanted is from a living donor. There’s a separate set of guidelines about choosing a living donor’s kidney than there is for that of a deceased donor.  

By the way, my use of term ‘cadaver donor’ last week created quite a controversy, so I went to a newly discovered site for me, Gift of Life, to find acceptable terms. The one I should have used is ‘deceased.’ My sincerest apologies to those who I inadvertently offended. 

Back to the guidelines for living kidney donation. Let’s find out about them together. First, I’d like to know more about what living kidney donation is. The National Kidney Foundation, my constant favorite source of anything kidney, explains: 

“Living donation takes place when a living person donates an organ (or part of an organ) for transplantation to another person. The living donor can be a family member, such as a parent, child, brother or sister (living related donation). 

Living donation can also come from someone who is emotionally related to the recipient, such as a good friend, spouse or an in-law (living unrelated donation). Thanks to improved medications, a genetic link between the donor and recipient is no longer required to ensure a successful transplant. 

In some cases, living donation may even be from a stranger, which is called anonymous or non-directed donation.” 

Got it. I went to another trusted source, the American Kidney Fund, to find out a bit about what would qualify you to be a living kidney donor. 

“If you want to be a living donor, you will need to have a medical exam with blood tests to be sure you are healthy enough to donate a kidney. Some of the tests needed may include: 

Blood tests 

Urine tests 

Pap smear/ gynecological exam 

Colonoscopy (if over age 50) 

Screening tests for cancer 

Antibody test 

X-ray 

Electrocardiogram (EKG) which looks at your heart 

Other image testing like a CT scan 

You are also required to meet with a psychologist and an Independent Living Donor Advocate to be sure you are mentally and emotionally ready to donate one of your kidneys. 

If you are found to be healthy, and your antibodies and blood type are well-matched to the person getting your kidney, you may be approved to donate your kidney.” 

Who better than the Living Kidney Donors Network to explain why a living kidney donation is preferred over a deceased kidney donation. 

“Kidney transplants save and improve the lives of people with kidney failure. Kidney donation from deceased donors has not been able to keep up with the need for kidney transplants. Over 5,000 people die every year waiting for a kidney transplant.  
Living kidney donation has revolutionized kidney transplantation and is now preferred when compared to a deceased donor transplant. Several benefits and advantages of living donation are now recognized:  

  • Living donation eliminates the recipient’s need for placement on the national waiting list. 
  • Short and long term survival rates are significantly better for transplants from living donors than transplants from deceased donors. (On average, approximately 18 years for a kidney from a living donor compared to 13 years for a kidney from a deceased donor). 
  • The recipients knows the donor, his/her lifestyle choices and medical history 
  • Living donor kidneys almost always start functioning immediately, whereas deceased donor kidneys can take from a few days to a few weeks to start functioning. (Often called a Sleepy Kidney) 
  • Shortens the waiting time for others on the waiting list. 
  • Health deteriorates the longer someone remains on dialysis. 
  • A kidney transplant doubles the life expectancy compared to staying on kidney dialysis treatment. 
  • May be able to avoid being on dialysis 
  • The recipient has time to plan for the transplant 
  • Waiting for a deceased donor can be very stressful and unhealthy. 
  • The surgery can be scheduled at a mutually-agreed upon time rather than performed on an emergency basis. 

Perhaps the most important aspect of living donation is the psychological benefit. The recipient can experience positive feelings knowing that the gift came from a loved one or a caring stranger. The donor experiences the satisfaction of knowing that he or she has contributed to the improved health of the recipient.” 

I wasn’t sure about antibodies although I know what they are and have heard of them in relation to living kidney donors. Johns Hopkins, another source I often turn to, had an explanation I could understand.  

“To test a recipient for these antibodies, a sample of their blood is mixed with a sample of the potential donor’s blood. This test is called a ‘crossmatch,’ and shows how a recipient’s antibodies react with the potential donor’s. Test results can be either positive or negative. It may seem confusing at first, but a positive crossmatch means that a donor and recipient are not compatible. 

A positive crossmatch results in the recipient’s antibodies attacking the donor’s which means the kidney is not suitable for transplant. 

A negative crossmatch means that the recipient’s antibodies do not attack the donor’s which means the kidney is suitable for transplant…. 

If a donor and recipient are not compatible, a transplant can still be performed. Experts at the Johns Hopkins Comprehensive Transplant Center developed a method call plasmapheresis, which helps make a kidney more compatible for a recipient and significantly affects survival outcomes.” 

As you can see from today’s blog, this is a complex matter. We have only touched upon what needs to be involved with a living donor kidney transplant. To further complicate matters, there are two distinct kinds of living donor kidney transplants as UNOS, the site of the United Network for Organ Sharing, tells us: 

“Directed donation 

In a directed donation, the donor names the specific person to receive the transplant. This is the most common type of living donation. The donor may be: 

a biological relative, such as a parent, brother, sister or adult child, 

a biologically unrelated person who has a personal or social connection with the transplant candidate, such as a spouse or significant other, a friend or a coworker, or 

a biologically unrelated person who has heard about the transplant candidate’s need. 

If tests reveal that the donor would not be a good medical match, paired donation may be an option. 

Paired donation 

Sometimes a transplant candidate has someone who wants to donate a kidney to them, but tests reveal that the kidney would not be a good medical match. Kidney paired donation, or KPD, also called kidney exchange, gives that transplant candidate another option. In KPD, living donor kidneys are swapped so each recipient receives a compatible transplant. 

For example, in the diagram above, Barbara wants to donate to her sister Donna, but they do not have matching blood types. Carlos wants to donate to his wife Maria, but they are also not compatible. By ‘swapping’ donors so that Carlos matches Donna and Barbara matches Maria, two transplants are made possible. This type of exchange often involves multiple living kidney donor/transplant candidate pairs.” 

 While today’s blog is longer than usual, there’s still more information we need to know about kidney transplants. There are now 90,872 people [about the seating capacity of the Los Angeles Memorial Coliseum] in the United States awaiting a kidney transplant. That is an astounding number. National Donate Life Month is turning out to be a learning experience for me as well as you. 

Until next week, 

Keep living your life! 

Dying is Not the End

Unbeknownst to me until I started researching kidney transplant, there is a National Donor Day. According to DonateLife

“Observed every year on February 14th, National Donor Day is an observance dedicated to spreading awareness and education about organ, eye and tissue donation. By educating and sharing the Donate Life message, we can each take small steps every day to help save and heal more lives, and honor the donor’s legacy of generosity and compassion. National Donor Day is a time to focus on all types of donation—organ, eye, tissue, blood, platelets and marrow. Join us by participating in local events, sharing social media messages and encouraging others to register as donors. 

National Donor Day is also a day to recognize those who have given and received the gift of life through organ, eye and tissue donation, are currently waiting for a lifesaving transplant, and those who died waiting because an organ was not donated in time.” 

I would suspect it’s no accident that this is celebrated on Valentine’s Day. 

On to cadaver donor, as promised last week. I’ve been perusing kidney transplant social media sites this past week and found lots of questions by those considering, and meeting the conditions for, a kidney transplant. A number of them wanted to know the difference between a cadaver transplant and a living donor transplant. It’s not as obvious as you might think. 

A cadaver transplant comes from a cadaver, or dead body, as you’ve probably figured out. Sometimes it’s called a deceased or non-living donor transplant. But what are the guidelines for which kidneys are useable and which are not?  Let’s see if the Donor Alliance can help us out with some general background information. 

“Kidney allocation is heavily influenced by waiting time, or how long the recipient has been listed for transplant. Fortunately there is a bridge treatment for many in end-stage renal disease, called dialysis, which allows candidates to survive while awaiting a transplant. In addition, blood type and other biological factors, as well as body size of the donor and recipient are always key factors. Medical urgency and location are also factors but less so than other organs as they [sic] kidney can remain viable outside the body for 24-36 hours under the proper conditions. 

The waiting list is not simply a list of people who are eligible for transplant. It’s a dynamic, complex algorithm based on carefully developed policy that ensures scarce organs are allocated to recipients as fairly and accurately as possible within highly constricted time frames.” 

Okay, so one guideline for a cadaver kidney is that it can remain alive outside the body for 24-36 hours. That seems to indicate, as mentioned above, that the location of both the donor and recipient are important, even though that’s fairly long for cadaver organs. 

I was surprised to learn that there are different types of deceased donor transplants.  

“A deceased donor is an individual who has recently passed away of causes not affecting the organ intended for transplant. Deceased donor organs usually come from people who have decided to donate their organs before death by signing organ donor cards. Permission for donation also may be given by the deceased person’s family at the time of death. 

A deceased donor kidney transplant occurs when a kidney is taken from a deceased donor and is surgically transplanted into the body of a recipient whose natural kidneys are diseased or not functioning properly. 

Types of Deceased Donor Organs 

There are several different types of deceased donor kidneys. These names are used to describe certain anatomic, biological, and social features of the donor organs. You may decide not to receive any or all of these organs, and you may change your mind at any time. 

Standard Criteria Donors (SCD): These kidneys are from donors under age 50 and do not meet any of the criteria below that are assigned to Expanded Criteria Donors. 

Expanded Criteria Donors (ECD): These organs come from donors over age 60 or age 50-59 that also have at least two of the following criteria – history of high blood pressure, the donor passed away from a CVA (stroke) or had a creatinine higher than the normal laboratory value (1.5 mg/dl). About 15-20% of the donors in the United States are Expanded Criteria. 

Donation after Cardiac Death (DCD): These donors do not meet the standard criteria for brain death. Their hearts stopped before the organs were removed. Donation after Cardiac Death occurs when continuing medical care is futile, and the donor patient is to be removed from all medical life-sustaining measures/supports. 

Double Kidney Transplants (Duals): During the year we may have access to donors that are at the more extreme limit of the Expanded Criteria Donor. Research has found that using both of these kidneys in one recipient is preferable to only one. 

Donors with High-Risk Social Behavior: These donors are individuals who at some point in their life practiced high-risk behavior for sexually transmitted disease, drug use, or were incarcerated. All of these donors are tested for transmissible disease at the time of organ recovery. You will be informed of the high-risk behavior. 

All of these kidneys supply suitable organs for transplant, and all are expected to provide good outcomes with good organ function. However, the outcomes may be 5-10% less than that achieved with Standard Criteria organs. Accepting a kidney that is not considered Standard Criteria may substantially reduce your waiting time.” 

Thank you to one of my favorite sources, the Cleveland Clinic for this information. 

While this is not all the information available about deceased kidney donors, I think it’s important to know how to register to be a donor. I registered when I had my first child. Her birth had gotten me to thinking about helping others. 

The Health Resources and Service Administration’s OrganDonor.gov provides the easiest two ways: 

“Signing up on your state registry means that someday you could save lives as a donor—by leaving behind the gift of life. When you register, most states let you choose what organs and tissues you want to donate, and you can update your status at any time.” 

There is a download for your state on their site. The other way is: 

“…in-person at your local motor vehicle department.” 

You know which I hope you choose in the time of Covid. 

I chose to donate my body to science. MedCure is the organization that clinched my decision for me. 

“Everything we know about the human body comes from studying whole body donors. At MedCure, we connect you or your loved ones to the physicians, surgeons, and researchers who are continuing this vital work. Their discoveries and innovations help people live longer, make treatments less invasive, and create new ways to prevent illness or disease. 

We are constantly overwhelmed by the incredible generosity and selflessness of our donors.  MedCure honors their gifts by covering, upon acceptance, all expenses related to the donation process. These costs include transportation from the place of passing, cremation, and a certified copy of the death certificate, as well as the return of cremated remains to the family or a scattering of the ashes at sea. By request, we can provide a family letter that shares more detailed information on how you or your loved one contributed to medical science.” 

Whichever you chose, thank you for saving lives one way or another. 

Until next week, 

Keep living your life! 

Giving It Away

Good-bye to National Kidney Month and a belated hello to National Donor Month. I don’t usually write about transplants and don’t know that much about them, so you and I will be learning together today. Restricting this blog to solely kidney transplants, there’s still quite a bit to write about. 

There are many reasons for needing a kidney transplant. The U.S. Department of Health & Human Services’s Health Resources & Services Administration’s Organ Procurement and Transplantation Network provides the following list of reasons: 

Kidney Diagnosis Categories>Kidney Diagnoses
GLOMERULAR DISEASESAnti-GBM; Chronic Glomerulonephritis: Unspecified; Chronic Glomerulosclerosis: Unspecified; Focal Glomerularsclerosis; Idio/Post-Inf Crescentic; Glomerulonephritis; IGA Nephropathy; Hemolytic Uremic Syndrome; Membranous Glomerulonephritis; Mesangio-Capillary 1 Glomerulonephritis; Mesangio-Capillary 2 Glomerulonephritis; Systemic Lupus Erythematosus; Alport’s Syndrome; Amyloidosis; Membranous Nephropathy; Goodpasture’s Syndrome; Henoch-Schoenlein Purpura; Sickle Cell Anemia; Wegeners Granulomatosis
DIABETESDiabetes: Type I Insulin Dep/Juvenile Onset; Diabetes: Type II Insulin Dep/Adult Onset; Diabetes: Type I Non-insulin Dep/Juv Onset; Diabetes: Type II Non-insulin Dep/Adult Onset
POLYCYSTIC KIDNEYSPolycystic Kidneys
HYPERTENSIVE NEPHROSCLEROSISHypertensive Nephrosclerosis
RENOVASCULAR AND OTHER VASCULAR DISEASESChronic Nephrosclerosis: Unspecified; Malignant Hypertension; Polyarteritis; Progressive Systemic Sclerosis; Renal Artery Thrombosis; Scleroderma
CONGENITAL, RARE FAMILIAL, AND METABOLIC DISORDERSCongenital Obstructive Uropathy; Cystinosis; Fabry’s Disease; Hypoplasia/Dysplasia/Dysgenesis/Agenesis; Medullary Cystic Disease; Nephrophthisis; Prune Belly Syndrome
TUBULAR AND INTERSTITIAL DISEASESAcquired Obstructive Nephropathy; Analgesic Nephropathy; Antibiotic-induced Nephritis; Cancer Chemotherapy-Induced Nephritis; Chronic Pyelonephritis/Reflex; Nephropathy; Gout; Nephritis; Nephrolithiasis; Oxalate Nephropathy; Radiation Nephritis; Acute Tubular Necrosis; Cortical Necrosis; Cyclosporin Nephrotoxicity; Heroin Nephrotoxicity; Sarcoidosis; Urolithiasis
NEOPLASMSIncidental Carcinoma; Lymphoma; Myeloma; Renal Cell Carcinoma; Wilms’ Tumor
RETRANSPLANT/GRAFT FAILURERetransplant/Graft Failure
OTHEROther Rheumatoid Arthritis; Other Familial Nephropathy

Quite a few of these reasons should look familiar to you if you’ve been reading the blog regularly since I’ve written about them. You can use the topics dropdown to the right of the blog if you’d like to refresh your memory about specific reasons. 

Let’s take a look at some astounding numbers. Unfortunately, The National Kidney Foundation could only offer statistics from 2014. Very few sources separate donations specifically by organ, so we’re lucky to have even these older numbers.  

“There are currently 121,678 people waiting for lifesaving organ transplants in the U.S. Of these, 100,791 await kidney transplants. (as of 1/11/16) … 

The median wait time for an individual’s first kidney transplant is 3.6 years and can vary depending on health, compatibility and availability of organs … 

In 2014, 17,107 kidney transplants took place in the US. Of these, 11,570 came from deceased donors and 5,537 came from living donors… 

On average: 

Over 3,000 new patients are added to the kidney waiting list each month… 

13 people die each day while waiting for a life-saving kidney transplant… 

Every 14 minutes someone is added to the kidney transplant list… 

In 2014, 4,761 patients died while waiting for a kidney transplant. Another, 3,668 people became too sick to receive a kidney transplant… “ 

Fewer kidney transplants are being performed during the current pandemic. The American Kidney Fund explains why: 

“Because living-donor kidney transplants require two hospital beds and post-surgical recovery care in the hospital, we are hearing that a growing number of transplant centers are temporarily putting living-donor transplants on hold. This both preserves the availability of hospital beds for emergencies and COVID-19 patients, and also keeps non-infected people out of the hospital…. 

The coronavirus spreads easily from person to person, and can be spread by people who do not show symptoms of COVID-19. This puts anyone who has a compromised immune system—including transplant patients who take immunosuppressive drugs—at an increased risk of becoming infected. 
 
Even with social distancing, the virus is still spreading in communities. Newly transplanted patients would be especially vulnerable during their recovery period after transplant surgery. 
 
Another obstacle hospitals face is the need to test deceased donors for the coronavirus. Transplanting an organ from a coronavirus-positive patient could present a grave risk to the recipient. With limited test kits needed for living patients, and the lag time between testing and getting results, some hospitals may have to forgo testing—and procuring organs from—deceased donors…. 

Because COVID-19 is a serious respiratory illness, the most critical patients must be put on ventilators. Ventilators are normally used to keep an organ donor patient alive who is medically brain-dead so that their organs may be removed and transplanted. Those ventilators may be needed for COVID-19 patients instead….” 

Fewer transplants or not, I was curious about how it’s decided who is eligible for a kidney transplant. Nebraska Medicine had the answer in simple terms we can all understand: 

“In order to be eligible to receive a kidney transplant: 

You must have chronic irreversible kidney disease that has not responded to other medical or surgical treatments. You are either on dialysis or may require dialysis in the near future. 

You must qualify for and be able to tolerate major surgery. 

You and your family members/support system must be able to understand the risks and benefits of transplantation, including the long-term need for close medical follow-up and lifelong need for anti-rejection therapy. 

You and your family must be able to accept the responsibilities, including financial, that are part of the long-term care you will need after transplantation. 

Exclusion 

You may not be eligible to receive a kidney transplant due to: 

The presence of some other life-threatening disease or condition that would not improve with transplantation. This could include certain cancers, infections that cannot be treated or cured, or severe, uncorrectable heart disease. 

A history of chronic noncompliance including, but not limited to, medical treatments, medications or other behaviors that would affect your ability to fully care for yourself after transplantation. 

A history of chronic and ongoing drug and/or alcohol abuse that cannot be successfully treated before transplantation, putting you at risk for continued harmful behavior after transplantation. 

A history of serious psychiatric disorders that cannot be successfully treated before transplantation, and that would be considered a high risk for ongoing or increased severity of the psychiatric disorder after transplantation.” 

Note: Weight is included in your tolerability for major surgery. 

There’s so much more to write about re kidney transplant. Next week, we’ll talk about the process itself. 

Until next week, 

Keep living your life! 

Almost the End of National Kidney Month 

Today we have the fifth National Kidney Month blog. You know, it’s also National Women’s Month. What better way to celebrate both than to write about women in nephrology?  I had intended to complete multiple searches for this information, but it looks like Martín-Gómez MA, García Agudo R, and Arenas Jiménez MD beat me to it with their paper El papel de la mujer a lo largo de la historia de la Nefrología which appeared in Nefrologia. 2019;39:15–17.  

In English rather than its original Spanish, the title is The role of women throughout the history of Nephrology. As a woman and a Chronic Kidney Disease writer, I owe them a huge debt of gratitude. Here are the parts of their paper pertaining to individual women in nephrology: 

“Dr Josephine Briggs, responsible for research at the US National Institutes of Health in the 1990s on the renin-angiotensin system, diabetic nephropathy, blood pressure and the effect of antioxidants in kidney disease. 

Dr Renée Habib (France), a pioneer of nephropathology [Gail here: that means disease or damage of the kidneys.] in Europe. She worked with the founders of the ISN to establish nephrology as a speciality. 

Dr Vidya N Acharya, the first female nephrologist in India inspiring the study of kidney diseases, dedicating her research to urinary infections and heading a Nephrology department in Mumbai. 

Dr Hai Yan Wang, head of department and professor of Nephrology at the Peking University First Hospital since 1983, president of the Chinese Society of Nephrology and editor of Chinese and international nephrology journals. 

Dr Mona Al-Rukhaimi, co-president of the ISN and leader of the working group on the KDIGO guidelines in the Middle East, as well as a participant in the Declaration of Istanbul on Organ Trafficking and Transplant Tourism. 

Dr Saraladevi Naicker, who created the first training programme [sic]for nephrologists in Africa and the Kidney Transplant Unit at Addington Hospital. 

Dr Batya Kristal, the first woman to lead a Nephrology department in Israel and founder of Israel’s National Kidney Foundation. She conducts her current research in the field of oxidative stress and inflammation. 

Dr Priscilla Kincaid-Smith, head of Nephrology at Melbourne Hospital, where she promoted the relationship between hypertension and the kidney and analgesic nephropathy. The first and only female president of the ISN, she empowered many other women, including the nephrologist Judy Whitworth, chair of the World Health Organization committee…. 

Dr M. Teresa D’Ocón Asensi, the first female head of the Nephrology Department at the Hospital San Carlos in Madrid since it was founded in 1962 and designer of a conservative prosthesis of the peritoneal catheter tract based on urological plugs. She was the only female member of the board of directors of the SEN (Sociedad Española de Nefrología [Spanish Society of Nephrology]) since its formation in 1964, until 1976.  

Women were not represented again in the management of the Spanish society until 1987, with the figure of Dr M. Dolores Jarillo Ibáñez (1987–1993)…. 

Dr María Teresa González, creator of the first nephrology and diabetes clinic at the Hospital de Bellvitge, in 1978. 

Dr Dolores Prats, who promoted peritoneal dialysis and studies on permeability and duration of the peritoneal membrane at the Hospital Clínico in Madrid. She succeeded her female predecessor as head of department, following said predecessor’s death in 1981. 

Dr Ana Gonzalo Fondona, who performed the first studies on complement activation in glomerulopathies at the Hospital de Bellvitge…. 

Isabel Entero, creator of the Fundación Renal Íñigo Álvarez de Toledo, founder of ALCER (Asociación para la Lucha Contra las Enfermedades de Riñón [Spanish Association for the Fight Against Kidney Diseases]) in 1976 and participant in the Transplant Act in 1979 

Dr Blanca Miranda, who replaced Isabel Entero as director of said Foundation from 1982, formed part of the drafting committee of the journal Nefrología from 1995 and coordinator of the Spanish National Transplant Organisation between 1996 and 2004. 

The journal Nefrología, which was created in 1981 by Dr Luis Hernando, did not include women on the editorial board until 1989: Dr Nieves Gallego, Dr Emma Huarte and Dr Dolores Jarillo….” 

You’ll notice the paper was printed in the beginning of 2019, so I decided to add more current women in nephrology. 

Dr. Vanessa Grubb first approached me when she was considering writing a blog herself. I believe she’s an important woman nephrologist since she has a special interest in the experiences of Black kidney patients. Here is what University of California’s Department of Medicine’s Center for Vulnerable Populations lists for her: 

“Dr. Vanessa Grubbs is an Associate Professor in the Division of Nephrology at UCSF and has maintained a clinical practice and research program at Zuckerberg San Francisco General Hospital since 2009. Her research focuses on palliative care for patients with end-stage kidney disease. She is among the 2017 cohort for the Cambia Health Foundation Sojourns Scholar Leadership Program, an initiative designed to identify, cultivate and advance the next generation of palliative care leaders; and the 2018 California Health Care Foundation’s Health Care Leadership Program. 
 
Her clinical and research work fuel her passion for creative writing. Her first book, HUNDREDS OF INTERLACED FINGERS: A Kidney Doctor’s Search for the Perfect Match, was released June 2017 from Harper Collins Publishers, Amistad division and is now in paperback.” 

I think Dr. Li-li Hsiao should also be included in today’s blog since she has a special interest in the Asian community and their experiences with kidney disease. The following is from the Boston Taiwanese Biotechnological Association:  

“…. She is the Director of Asian Renal Clinic at BWH; the co-program director and Co-PI of Harvard Summer Research Program in Kidney Medicine. She is recently appointed as the Director of Global Kidney Health Innovation Center. Dr Hsiao’s areas of research include cardiovascular complications in patients with chronic kidney disease; one of her work published in Circulation in 2012 has been ranked at the top 1% most cited article in the Clinical Medicine since 2013. Dr. Hsiao has received numerous awards for her outstanding clinical work, teaching and mentoring of students including Starfish Award recognizing her effective clinical care, and the prestigious Clifford Barger Mentor Award at HMS. Dr. Hsiao is the founder of Kidney Disease Screening and Awareness Program (KDSAP) at Harvard College where she has served as the official advisor. KDSAP has expanded beyond Harvard campus. Dr. Hsiao served in the admission committee of HMS; a committee member of Post Graduate Education and the board of advisor of American Society of Nephrology (ASN). She was Co-Chair for the ‘Professional Development Seminar’ course during the ASN week, and currently, she is the past-president of WIN (Women In Neprology [sic]).   

I don’t believe we, as women, will continue to be underrepresented in the nephrology community for very much longer. 

Until next week, 

Keep living your life! 

SLOWITDOWNCKD News

Digitally available on Amazon today! Print copy coming soon. So glad I was able to get this out during National Kidney Month!!!

Published in: on March 22, 2021 at 5:07 pm  Leave a Comment  

What’s New?

Here we are in the fourth week of National Kidney Month. I caught myself wondering if I were up to date on anything and everything new in the world of kidney disease. I receive emails every day about this or that happening in the kidney community, but how many of them refer to what’s new? I decided to find out. 

I started with a general search and found quite a bit. Let’s start with this paper which was published on January 5th of this year. Since I’ve just had an expensive new crown made, this one on ScienceDaily caught my eye: 

“Lead author Dr Praveen Sharma, from the Periodontal Research Group at the University of Birmingham’s School of Dentistry, said: ‘This is the first paper to quantify the causal effect of periodontitis on kidney function and vice-versa as well as the first to elucidate the pathways involved. 

It showed that even a modest reduction in gum inflammation can benefit renal function. Given the relative ease of achieving a 10% reduction in gum inflammation, through simple measures like correct brushing techniques and cleaning between the teeth, these results are very interesting.’ ” 

Reminder: periodontis is gum infection which can become so serious that you lose teeth and possibly even affects the bone under your teeth. The ‘dont’ part of the word means teeth, while ‘peri’ means around. By this time in reading the blog, we can figure out that ‘itis’ means inflammation. Keep up the brushing and flossing, folks. This may help you save your kidneys. 

Just a week later, on January 12th, EuerkAlert! announced: 

“While investigating the underlying causes of a rare skin disorder, a researcher at Massachusetts General Hospital (MGH) discovered a previously unknown mechanism in the kidneys that is important for regulating levels of magnesium and calcium in the blood. 

The discovery, described in the journal Cell Reports, highlights the role of a previously little-studied gene called KCTD1. The gene directs production of a protein that regulates the kidney’s ability to reabsorb magnesium and calcium from urine and return it to the bloodstream.” 

According to the U.S. Department of Health and Human Service’s National Institutes of Health’s Office of Dietary Supplements,  

“Magnesium is a nutrient that the body needs to stay healthy. Magnesium is important for many processes in the body, including regulating muscle and nerve function, blood sugar levels, and blood pressure and making protein, bone, and DNA.” 

According to the same agency

“The body needs calcium to maintain strong bones and to carry out many important functions. Almost all calcium is stored in bones and teeth, where it supports their structure and hardness. 

The body also needs calcium for muscles to move and for nerves to carry messages between the brain and everybody part. In addition, calcium is used to help blood vessels move blood throughout the body and to help release hormones and enzymes that affect almost every function in the human body.” 

I remember being flabbergasted upon discovering that the kidneys produce glucose. Can you imagine how my mind is reeling to learn that it also regulates the levels of magnesium and calcium in the blood? Maybe instead of telling me to drink my milk for calcium, my mom should have been telling me to keep an eye on my kidney function… not that we even knew what the kidneys were back then. [By we, I mean my mom and me.] 

But wait, there’s more. [Why do I feel like a 2 a.m. television ad?] Many important discoveries started as experiments with fruit flies. Hopefully, this one announced on January 26th is another of those: 

“In a new paper published in the journal Molecules, alum Cassandra Millet-Boureima (MSc 19) and Chiara Gamberi, affiliate assistant professor of biology, write that melatonin was found to reduce cysts in the renal tubules of fruit flies. These tubules are also found in more complex mammals, including humans, where they are called nephrons. This study, which builds on previous studies by Millet-Boureima and Gamberi, was co-authored by Roman Rozencwaig and Felix Polyak of BH Bioscience in Montreal. 

The researchers hope that their findings can be applied to treating people suffering from autosomal dominant polycystic kidney disease. ADPKD is a genetic chronic and progressive disease characterized by the growth of dozens of cysts in the nephrons. It is incurable and affects approximately 12.5 million worldwide.” 

Thank you to Medical Dialogues for this information. You may need a reminder about ADPKD, so here it is from PDK Foundation

“Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common, life-threatening genetic diseases. In ADPKD, fluid-filled cysts develop and enlarge in both kidneys, eventually leading to kidney failure.” 

May as well define melatonin, too, don’t you think? My favorite dictionary helped us out here: 

“a vertebrate hormone that is derived from serotonin, is secreted by the pineal gland especially in response to darkness, and has been linked to the regulation of circadian rhythms.” 

We are vertebrates, meaning we have a backbone. The pineal gland is sometimes called the third eye, which makes sense now since it responds to darkness, just as our eyes do. 

There are a few more just this year alone, but I think we have room for just one more in today’s blog. 

“Oxygen is essential for human life, but within the body, certain biological environmental conditions can transform oxygen into aggressively reactive molecules called reactive oxygen species (ROS), which can damage DNA, RNA, and proteins. Normally, the body relies on molecules called antioxidants to convert ROS into less dangerous chemical species through a process called reduction. But unhealthy lifestyles, various diseases, stress, and aging can all contribute to an imbalance between the production of ROS and the body’s ability to reduce and eliminate them. The resulting excessive levels of ROS cause ‘oxidative stress,’ which can disrupt normal cellular functions and increase the risk of diseases like cancer, neurodegeneration, kidney dysfunction, and others, which are all accompanied by severe inflammation. 

Since oxidative stress is associated with various serious diseases, its detection within living organs offers a route to early diagnosis and preventive treatment, and is, thus, a matter of considerable interest to scientists working in the field of biomedicine. Recent international collaboration between the Japanese National Institutes for Quantum and Radiological Science and Technology (QST), Bulgarian Academy of Sciences, and Sofia University St. Kliment Ohridski in Bulgaria led to a promising technology for this purpose: a novel quantum sensor. Their work is published in the scientific journal Analytical Chemistry2021.” 

This was from their January 29th press release. Here we have another valuable theory of inquiry. 

My head is swimming. There’s so much new research re keeping our kidneys healthy. 

Until next week, 

Keep living your life! 

National Kidney Month

The world has acknowledged World Kidney Day. We have had walks in many countries. We have had educational seminars in many countries. We have posted in many countries. All to bring awareness to what our kidneys do for us and the worldwide challenge of kidney disease. Thursday, March 11th, was World Kidney Day. 

But today is Monday. And you know what? It’s still March, National Kidney Month, here in the United States. Each year, I write about National Kidney Month, just as I write about World Kidney Day. Interesting tidbit: the Philippines also has a National Kidney Month which they celebrate in June. I’ll only be writing about the U.S.’s National Kidney Day. 

 As usual, let’s start at the beginning. What is National Kidney Month? Personalized Cause has a succinct explanation for us. While I’m not endorsing them since I usually try to avoid endorsements, I do want to let you know they sell the green ribbons and wristbands for kidney disease awareness that you’ll probably be seeing hither and yon all month. 

“National Kidney Month, observed in March and sponsored by the National Kidney Foundation, is a time to increase awareness of kidney disease, promote the need for a cure, and spur advocacy on behalf of those suffering with the emotional, financial and physical burden of kidney disease. The National Kidney Foundation is the leading organization in the U.S. dedicated to the awareness, prevention and treatment of kidney disease for hundreds of thousands of healthcare professionals, millions of patients and their families, and tens of millions of Americans at risk. 

National Kidney Month is a time to increase awareness about the function of the kidneys and kidney disease. Kidneys filter 200 liters of blood a day, help regulate blood pressure and direct red blood cell production. But they are also prone to disease. One in three Americans is at risk for kidney disease due to diabetes, high blood pressure or a family history of kidney failure. There are more than 26 million Americans who already have kidney disease, and most do not know it because there are often no symptoms until the disease has progressed.” 

That, of course, prompted me to go directly to the National Kidney Foundation’s information about National Kidney Month. This is what I found: 

March 1, 2021, New York, NY — In honor of National Kidney Month which starts today, the National Kidney Foundation’s (NKF) national public awareness campaign, “Are You the 33%?” enters a new phase focusing on the connection between type 2 diabetes (T2D) and kidney disease, also known as chronic kidney disease (CKD). NKF urges everyone to find out if they’re the 1 in 3 at risk for developing kidney disease by taking a one-minute quiz at MinuteForYourKidneys.org

Diabetes is a leading risk factor for developing kidney disease. Over time, having high blood sugar from diabetes can cause damage inside your kidneys. But it doesn’t have to end up this way; because with careful control of glucose (sugar) levels, there is evidence that you can prevent kidney disease in people with diabetes. 

Award-winning actress, Debbie Allen joined the campaign as the T2D Campaign Celebrity Spokesperson in February, Black History Month, to help promote awareness of diabetes as a leading cause for developing chronic kidney disease. Allen has a family history of diabetes and was recently diagnosed with pre-diabetes.” 

Indeed, the National Kidney Foundation has a lot to offer with peer mentoring, community, an information helpline, and transplant, palliative care, dialysis, kidney donation, and research information. 

The American Kidney Fund [AFK] joins in National Kidney Month with their form to pledge to fight kidney disease. I signed up; you can, too, if you’d like to. I’m not comfortable with the word “fight,” but I’m not going to let that stop me from spreading awareness of the disease.  

If you’re inclined to donate to the cause, the American Kidney Fund is doubling your donation this month. They also offer an advocacy program, as well as free screenings, activity days, financial assistance, and kidney education in addition to transplant and kidney donation information, 

The National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK], part of the National Institutes of Health [NIH], celebrates National Kidney Month with the following post and offerings. 

“Follow these healthy lifestyle tips to take charge of your kidney health. 

  1. Meet regularly with your health care team. Staying connected with your doctor, whether in-person or using telehealth via phone or computer, can help you maintain your kidney health. 
  1. Manage blood pressure and monitor blood glucose levels. Work with your health care team to develop a plan to meet your blood pressure goals and check your blood glucose level regularly if you have diabetes. 
  1. Take medicine as prescribed and avoid NSAIDs like ibuprofen and naproxen. Your pharmacist and doctor need to know about all the medicines you take. 
  1. Aim for a healthy weight. Create a healthy meal plan and consider working with your doctor to develop a weight-loss plan that works for you. 
  1. Reduce stress and make physical activity part of your routine. Consider healthy stress-reducing activities and get at least 30 minutes or more of physical activity each day. 
  1. Make time for sleep. Aim for 7 to 8 hours of sleep per night. 
  1. Quit smoking. If you smoke, take steps to quit. 

It may seem difficult, but small changes can go a long way to keeping your kidneys and you healthier for longer. 

Learn more about managing kidney disease 

As for me, I’ll continue to blog my brains out [just as I declared in last week’s blog] until more and more people are aware of the kidneys and kidney disease. Same goes for the Instagram, Facebook, Twitter, Pinterest, and LinkedIn accounts, and the SlowItDownCKD book series. It’s all about kidney disease. 

Until next week, 

Keep living your life! 

World Kidney Day, 2021

Will you look at that? The world keeps moving on, pandemic or not. And so, I recognize that Thursday of this week is World Kidney Day. In honor of this occasion, I’ve chosen to update whatever I’ve written about World Kidney Day before … now sit back and enjoy the read. 

…World Kidney Day? What’s that? I discovered this is a fairly new designation. It was only fifteen years ago that it was initiated. 

 According to http://worldkidneyday.org

“World Kidney Day is a global awareness campaign aimed at raising awareness of the importance of our kidneys.” 

Sound familiar? That’s where I’m heading with What Is It and How Did I Get It? Early Stage Chronic Kidney DiseaseSlowItDownCKD 2011SlowItDownCKD 2012

SlowItDownCKD 2013SlowItDownCKD 2014SlowItDownCKD 2015;

 SlowItDownCKD 2016SlowItDownCKD 2017

SlowItDownCKD 2018SlowItDownCKD 2019the soon to be published SlowItDownCKD 2020; Facebook; Instagram; LinkedIn; Pinterest; Twitter; and this blog. We may be running along different tracks, but we’re headed in the same direction. 

According to their website,  

The International Society of Nephrology (ISN) is a global professional association dedicated to advancing kidney health worldwide since 1960 through education, grants, research, and advocacy.  

We do this for all our stakeholders by:  

BRIDGING THE GAPS of available care through advocacy and collaborations with our global partners  

BUILDING CAPACITY in healthcare professionals via granting programs, education and research  

CONNNECTING OUR COMMUNITY to develop a stronger understanding of the management of kidney disease.  

The ISN, through its members and in collaboration with national and regional societies, engages 30,000 health professionals from across the globe to reduce the burden of kidney diseases and provide optimal health care for patients.”  

If you go to Initiatives on the ISN’s website, you’ll find the following: 

“World Kidney Day (WKD) is a joint initiative between the International Society of Nephrology (ISN) and the International Federation of Kidney Foundations (IFKF). 

World Kidney Day is a global campaign that aims to raise awareness of the importance of our kidneys to overall health and to reduce the frequency and impact of kidney disease and its associated health problems. 

World Kidney Day is an annual event that takes place worldwide. Hundreds of organizations and individuals launch initiatives and events on WKD to help raise awareness of kidney disease.” 

Now we just need to know what the International Federation of Kidney Foundations (IFKF) has to say about themselves: 

“Vision 

Better kidney health for all. 

Optimal care for people affected with Kidney Disease or Kidney Failure. 

Mission 

Leading a worldwide movement to 

Promote better kidney health with primary, secondary and tertiary preventive measures. 

Promote optimal treatment and care so as to maximize the health, quality of life, and longevity for people with or at high risk for developing Kidney Disease or Kidney Failure.” 

As of July of last year, the name has been changed to the International Federation of Kidney Foundations – World Kidney Alliance (IFKF-WKA) 

Photo by Karolina Grabowska on Pexels.com

Back to World Kidney Day’s website now, if you please. 

“The World Kidney Day Steering Committee has declared 2021 the year of ‘Living Well with Kidney Disease’. This has been done in order to both increase education and awareness about effective symptom management and patient empowerment, with the ultimate goal of encouraging life participation. Whilst effective measures to prevent kidney disease and its progression are important, patients with kidney disease – including those who depend on dialysis and transplantation – and their care-partners should also feel supported, especially during pandemics and other challenging periods, by the concerted efforts of kidney care communities.” 

Their site offers materials and ideas for events as well as a map of global events. Prepare to be awed at how wide spread World Kidney Day events are. 

Before you leave their page, take a detour to Kidney FAQ (Frequently Asked Questions) on the toolbar at the top of the page.  You can learn everything you need to know from what the kidneys do to what the symptoms (or lack thereof) of CKD are, from how to treat CKD to a toolbox full of helpful education about your kidneys to preventative measures. 

Just as this year’s, the previous World Kidney Day themes were all educational and much needed by the CKD community. 

“2020 Kidney Health for Everyone Everywhere – from Prevention to Detection and Equitable Access to Care 

2019 Kidney Health for Everyone, Everywhere 

2018 Kidneys & Women’s Health. Include, Value, Empower 

2017 Kidney Disease & Obesity – Healthy Lifestyle for Healthy Kidneys 

2016 Kidney Disease & Children – Act Early to Prevent It! 

2015 Kidney Health for All 

2014 Chronic Kidney Disease (CKD) and aging 

2013 Kidneys for Life – Stop Kidney Attack! 

2012 Donate – Kidneys for Life – Receive 

2011 Protect your kidneys: Save your heart 

2010 Protect your kidneys: Control diabetes 

2009 Protect your kidneys: Keep your pressure down 

2008 Your amazing kidneys! 

2007 CKD: Common, harmful and treatable 

2006 Are your kidneys OK?” 

If only my nurse practitioner had been aware of National Kidney Month [That’s the topic of next week’s blog] or World Kidney Day, she could have warned me immediately that I needed to make lifestyle changes so the decline of my kidney function could have been slowed down earlier. How much more of my kidney function would I still have if I’d known earlier? That was thirteen years ago. This shouldn’t still be happening… but it is. 

Photo by Gabby K on Pexels.com

I received a phone call a few years ago that just about broke my heart.  Someone very dear to me sobbed, “He’s dying.” When I calmed her down, she explained a parent was sent to a nephrologist who told him he has end stage renal disease and needed dialysis or transplantation immediately. 

I pried a little trying to get her to admit he’d been diagnosed before end stage, but she simply didn’t know what I was talking about. There had been no diagnose of Chronic Kidney Disease up to this point. There was diabetes, apparently out of control diabetes, but no one impressed upon this man that diabetes is the foremost cause of CKD. 

What a waste of the precious time he could have had to do more than stop smoking, which he did [to his credit], the moment he was told it would help with the diabetes.  Would he be where he was then if his medical practitioners had been aware of National Kidney Month or World Kidney Day, especially since this man was high risk due to his age and diabetes?  I fervently believe so. 

I have a close friend who was involved in the local senior center where she lives.  She said she didn’t know anyone else but me who had this disease.  Since 1 out of every 7 people does nationally (That’s 15% of the adult population) and being over 65 places you in a high risk group, I wonder how many of her friends were included in the 90% of those in the early stage of CKD who don’t know they have CKD or don’t even know they need to be tested.  I’d have rather been mistaken here, but I’m afraid I wasn’t. National Kidney Month or World Kidney Day could have helped them become aware. Thank you to the CDC for these figures. Please note the figures are as of 2019. 

For those of you who have forgotten [Easily understood explanations of what results of the different items on your tests mean are in What Is It and How Did I Get It? Early Stage Chronic Kidney Disease.], all it takes is a blood test and a urine test to detect CKD.  I have routine blood tests every three months to monitor a medication I’m taking.  It was in this test, a test I took anyway, that my family physician uncovered Chronic Kidney Disease as a problem. 

There is so much free education about CKD online. Maybe you can start with the blogroll on the right side of the blog or hit ‘Apps’ on the Topics Dropdown .Responsum is a good place to start. None of us needs to hear another sorrowful, “If only I had known!” 

Until next week, 

Keep living your life! 


What’s That Sound I Hear?

Ever since I had the surgery that removed part of my pancreas, my gall bladder, and my spleen while saving my life, I’ve had a superabundance of flatulence and belching. Remaining delighted that I’m alive, I’m still, well, embarrassed by this. I called the surgeon to see if this were normal. He hadn’t prescribed any long-term medication, so I think he was a bit surprised at my question. His answer was no. 

Hmmm, maybe it was another medication since medication can be the source of both belching and flatulence. I called all my other doctors (and there were plenty). Nope, no one had prescribed a medication that would cause this. I’m fairly careful with my diet, so what could be the cause? 

Ah, there I am starting in the middle again. Let’s go back to what each of these terms is. 

Scotland’s National Health Service Inform explains what flatulence is: 

“Flatulence is passing gas from the digestive system out of the back passage. [Gail here: I love how delicately that’s phrased.] It’s more commonly known as ‘passing wind,’ or ‘farting’. 

Farting is often laughed about, but excessive flatulence can be embarrassing and make you feel uncomfortable around others. However, it can usually be controlled with changes to your diet and lifestyle. 

Flatulence is a normal biological process and is something everyone experiences regularly. Some people pass wind only a few times a day, others a lot more, but the average is said to be about 5 to 15 times a day.” 

While I like how easily I understood the definition, I wanted a little bit more and to find out about belching, too. Fortis Memorial Research Institute helped here and even threw in a bit about bloating – which seems to go along with belching and flatulence. It also explained what the pain you might experience with these three is: 

“Belching is a normal process and results from swallowed air accumulating in the stomach. The [sic] can be subsequently passed as rectal gas (flatus) also. 

Bloating is the subjective feeling that the abdomen is full but does not necessarily mean that the abdomen is enlarged. 

Flatulence refers to the passage of rectal gas. The gas is generally a combination of swallowed air and gas produced by the action of colon bacteria on undigested food. 

Gas accumulation can lead to pain which could seem like gallbladder pain or pain that can radiate up to the chest and seem like cardiac pain.” 

This was more informative, but I still wanted to find out more about this subject. (I guess I’m just never satisfied!). The MayoClinic provided me with that: 

“Flatulence: Gas buildup in the intestines 

Gas in the small intestine or colon is typically caused by the digestion or fermentation of undigested food by bacteria found in the bowel. Gas can also form when your digestive system doesn’t completely break down certain components in foods, such as gluten, found in most grains, or the sugar in dairy products and fruit. 

Other sources of intestinal gas may include: 

Food residue in your colon 

A change in the bacteria in the small intestine 

Poor absorption of carbohydrates, which can upset the balance of helpful bacteria in your digestive system 

Constipation, since the longer food waste remains in your colon, the more time it has to ferment 

A digestive disorder, such as lactose or fructose intolerance or celiac disease” 

There must be a way to cut down on belching and flatulence, I thought. Even if it’s normal, maybe it doesn’t have to happen so very often. So, I turned to my old buddy, Everyday Health to see if I could find some of the causative behaviors: 

“Eating high-fiber foods like beans, legumes, fruits, vegetables, and whole grains 

Drinking carbonated beverages 

Chewing gum 

Eating too quickly or talking while chewing, which results in swallowing more air 

Drinking through a straw 

Consuming artificial sweeteners 

Chronic intestinal diseases like diverticulitis or inflammatory bowel disease 

Food intolerances like celiac disease or lactose intolerance 

Bacterial overgrowth in the small bowel” 

That sounds easy enough. Yet, something was missing for me. I’d had cancer and still have chronic kidney disease. Is there some kind of connection? I found none with cancer, but Kidney Health Australia did make the connection between chronic kidney disease, and belching, bloating, and flatulence. 

“Reduced kidney function can lead to bowel problems such as constipation and diarrhoea. This can cause stomach discomfort including pain, bloating, gas and nausea. A renal dietitian or renal nurse may be able to suggest how to safely increase the fibre in your diet. Gentle exercise such as walking can also help relieve discomfort. Medications can also provide relief.” 

It’s the gas you produce that causes bloating (sometimes), belching, and flatulence. Remember that the Mayo Clinic cited constipation can contribute to these. Now we find that “reduced kidney function” can lead to constipation. 

That’s what ckd is: a progression in the decline of your kidney function for at least three months. 

Your flatulence, bloating, and/or belching may also be a complication of another problem. Check in with your medical team. You have to remember that I am not a doctor and have never claimed to be one.  

Healthline suggests the following conditions may be the cause: 

“If your diet doesn’t contain a large amount of carbohydrates or sugars, and you don’t swallow excessive air, your excessive flatulence may be due to a medical condition. 

Potential conditions underlying flatulence range from temporary conditions to digestive problems. Some of these conditions include: 

constipation 

gastroenteritis 

food intolerances, such as lactose intolerance 

irritable bowel syndrome (IBS) 

Crohn’s disease 

celiac disease 

diabetes 

eating disorders 

ulcerative colitis 

dumping syndrome 

gastroesophageal reflux disease (GERD) 

autoimmune pancreatitis 

peptic ulcers” 

Uh-oh, did you notice “diabetes” in the list above? That’s the second most prevalent cause of CKD and vice-versa. 

Hopefully, today’s blog has told you everything you always wanted to know about ckd & flatulence, belching, and bloating, but were afraid to ask (with apologies to Woody Allen). 

Until next week, 

Keep living your life! 

Black History Month: Entertainers I Miss

This is the last week of Black History Month and I’d like to honor that. I’ve previously written about Blacks in the history of nephrology and other paths in life. Being a former actor and just having had a visit from a member of my acting community (a safe visit: double masked, hand sanitized, and social distanced.), I got to thinking about Blacks in entertainment who died of kidney disease.  

But first, this is what I included in the upcoming SlowItDownCKD 2020 to explain what Black History Month actually is: 

“As Andrea Wurtzburger wrote in People Magazine (I knew there was a reason I grabbed this first each time I waited in one medical office or another.) in the February 13, 2020… 

‘Black History Month is an entire month devoted to putting a spotlight on African Americans who have made contributions to our country. Originally, it was seen as a way of teaching students and young people about the contributions of Black and African Americans in school, as they had (and still have) been often forgotten or left out of the narrative of the growth of America. Now, it is seen as a celebration of those who’ve impacted not just the country, but the world with their activism and achievements.’” 

Now keep in mind that the further back we go, the more people there are that died of kidney disease since treatment was non-existent at first and then limited. Nephrology is a relatively young field of medicine. According to NEJM Resident 360, a nephrology journal for medical students, 

“The initial recognition of kidney disease as independent from other medical conditions is widely attributed to Richard Bright’s 1827 book ‘Reports of Medical Cases,’ which detailed the features and consequences of kidney disease. For the next 100 years or so, the term ‘Bright’s disease’ was used to refer to any type of kidney disease. Bright’s findings led to the widespread practice of testing urine for protein — one of the first diagnostic tests in medicine. 

The study of kidney disease was furthered by William Howship Dickinson’s description of acute nephritis in 1875 and Frederick Akbar Mahomed’s discovery of the link between kidney disease and hypertension in the 1870s. Mahomed’s original sphygmograph, created when he was a medical student, was improved in 1896 by Scipione Riva-Rocci, of Italy, with the use of a cuff to encircle the arm….” 

I’m listening to Art Tatum’s (10/13/09 – 11/5/56) music as I write today’s blog. According to National Public Radio (NPR): 

“One of the greatest improvisers in jazz history, Art Tatum also set the standard for technical dexterity with his classic 1933 recording of ‘Tea for Two.’ Nearly blind, Tatum had artistic vision and ability that made him an icon of jazz piano, a musician whose impact will be felt for generations to come…. 

Although his excessive drinking didn’t affect his playing, it did unfortunately affect his health. Tatum began showing evidence of euremia, a toxic blood condition resulting from a severe kidney disease. On Nov. 5, 1956, Tatum died at age 47, and although his career was relatively short, Tatum’s brilliant playing remains unparalleled and highly influential.” 

As far as I can tell, ‘euremia’ is either an alternative or misspelling of uremia. I could not find it despite multiple sources. Each one reverted to ‘uremia’. 

Have you heard of Ivan Dixon? No? How about the tv series ‘Hogan’s Heroes’? Encyclopedia.com organizes their information a bit differently: 

“Career: Stage, television, and screen actor, 1957-91; film and television director, 1970-93. 

Memberships: Academy of Motion Picture Arts and Sciences; Directors Guild of America; Negro Actors for Action; Screen Actors Guild. 

Awards: Emmy Award nomination, 1967, for The Final War of Olly Winter; received four National Association for the Advancement of Colored People Image Awards; Black Filmmakers Hall of Fame; National Black Theatre Award; Paul Robeson Pioneer Award, Black American Cinema Society. 

For his achievements on the stage and screen, Dixon was inducted into the Black Filmmakers Hall of Fame. He was the recipient of four National Association for the Advancement of Colored People Image Awards, in addition to the National Black Theatre Award and the Paul Robeson Pioneer Award given by the Black American Cinema Society.” 

He died of complications from kidney failure. There seems to be no record of what these complications were, although we can guess. 

Barry White (9/12/44 – 7/4/03), a singer and songwriter whose voice I will always miss, died of a stroke while awaiting a transplant. His kidney disease had been caused by hypertension.  The following is from Biography.com, which has much more information about him. 

“…. Love Unlimited’s success in 1972 can in large part be attributed to White’s throaty vocals in such hits as “Walkin’ In The Rain With The One I Love.” The group’s success rejuvenated White’s own career, receiving acclaim for such songs as “I’m Gonna Love You Just A Little More Baby” and “Never, Never Gonna Give Ya Up” in 1973 and “Can’t Get Enough Of Your Love, Babe” and “You’re The First, The Last, My Everything” in 1974…. 

During the peak of his career, White earned gold and platinum discs for worldwide sales. The UK singer Lisa Stansfield has often publicly supported White’s work and in 1992, she and White re-recorded a version of Stansfield’s hit, “All Around The World.” During the ’90s, a series of commercially successful albums proved White’s status as more than just a cult figure….” 

To be honest, the only way I could have enjoyed writing this blog more is if these talented people were still with us. 

Until next week, 

Keep living your life! 

Your Kidneys and Covid – or – Covid and Your Kidneys

Thanks to an unidentified woman at The Virginia G. Piper Cancer Center who passed a telephone number on to me, Bear and I have appointments for both our first and second Covid vaccinations. That got me to thinking. In this time of Covid with its breathing problems, is Chronic Kidney Disease involved in some way? We know that Covid can cause Acute Kidney Injury, but this is different. It’s trying to find out if CKD can contribute to Covid. 

Respiratory Acidosis sprang to mind, probably because of the word ‘respiratory.’ We already know acidosis can be a problem for CKD patients, but does it contribute to Covid? I didn’t know, so I started my search for an answer at The National Center for Biotechnology Information.    

“Acid-base disorders are common in patients with chronic kidney disease, with chronic metabolic acidosis receiving the most attention clinically in terms of diagnosis and treatment. A number of observational studies have reported on the prevalence of acid-base disorders in this patient population and their relationship with outcomes, mostly focusing on chronic metabolic acidosis…. “ 

Okay, so we’ve established chronic metabolic acidosis is common in CKD patients, but what is that? The National Kidney Foundation explains: 

“The buildup of acid in the body due to kidney disease or kidney failure is called metabolic acidosis. When your body fluids contain too much acid, it means that your body is either not getting rid of enough acid, is making too much acid, or cannot balance the acid in your body.” 

And, of course, we know that chronic means long term as opposed to acute, which means sudden onset. 

But respiratory acidosis? Is that part of acidosis? MedlinePlus came to the rescue with an easily understood definition for us: 

“Respiratory acidosis is a condition that occurs when the lungs cannot remove all of the carbon dioxide the body produces. This causes body fluids, especially the blood, to become too acidic.” 

Let me think a minute to figure out how this is all connected. Got it!  Let’s go back to what the kidneys do for us. 

“Your kidneys remove wastes and extra fluid from your body. Your kidneys also remove acid that is produced by the cells of your body and maintain a healthy balance of water, salts, and minerals—such as sodium, calcium, phosphorus, and potassium—in your blood. 

Without this balance, nerves, muscles, and other tissues in your body may not work normally. 

Your kidneys also make hormones that help 

  • control your blood pressure 
  • make red blood cells  
  • keep your bones strong and healthy” 

Thank you to the National Institute of Diabetes and Digestive and Kidney Diseases for the above information. 

Aha! Carbon dioxide is a waste product even though the body produces it. The kidneys are tasked with removing wastes. CKD is a progressive decline in your kidney function for over three months. Decline as in don’t work as well. Oh, my. CKD can contribute to breathing problems with Covid. 

The January, 2021, issue of NDT [ Gail here: that stands for Nephrology, Dialysis, Transplantation] tells us: 

“Although not listed in initial reports as a risk factor for severe COVID-19, CKD has emerged not only as the most prevalent comorbidity conveying an increased risk for severe COVID-19, but also as the comorbidity that conveys the highest risk for severe COVID-19. The increased risk is evident below the threshold of eGFR that defines CKD and the risk increases as the eGFR decreases, with the highest risk in patients on kidney replacement therapy. Although CKD patients are known to be at increased risk of death due to infectious diseases, the factors contributing to their greater vulnerability for severe COVID-19 should be explored, as these may provide valuable insights into therapeutic approaches to the disease in this patient group. It is presently unknown if earlier categories of CKD (G1/G2, i.e. patients with preserved kidney function but with increased albuminuria) are also at an increased risk of severe COVID-19, and this must be explored. Moreover, the recognition that CKD significantly contributes to the severity of COVID-19 should now result in focused efforts to improve outcomes for the 850 million global CKD patients.”  

Uh-oh, do we panic now? No, no, no.  We protect ourselves. The Centers for Disease Control and Prevention [CDC] has been extremely vocal about this: 

“It is especially important for people at increased risk of severe illness from COVID-19, and those who live with them, to protect themselves from getting COVID-19. 

The best way to protect yourself and to help reduce the spread of the virus that causes COVID-19 is to: 

Limit your interactions with other people as much as possible. 

Take precautions to prevent getting COVID-19 when you do interact with others. 

If you start feeling sick and think you may have COVID-19, get in touch with your healthcare provider within 24 hours.  If you don’t have a healthcare provider, contact your nearest community health center or health department.” 

The CDC further explains: 

“Three Important Ways to Slow the Spread 

Wear a mask to protect yourself and others and stop the spread of COVID-19. 

Stay at least 6 feet (about 2 arm lengths) from others who don’t live with you. 

Avoid crowds. The more people you are in contact with, the more likely you are to be exposed to COVID-19.” 

By the way, the CDC acknowledges that CKD raises your risk of getting Covid… as does diabetes… and possibly hypertension. These are also the two primary causes of CKD.  

Until next week,

Keep living your life!

It’s Not Just Scaly Patches

Did I ever mention that I have latent psoriasis? Or that it has something to do with Chronic Kidney Disease? Hmmm, well maybe it’s time… not that most people ever want to admit they have unsightly psoriasis. 

I realize not everyone knows what that is, so we’ll start with a definition from the Mayo Clinic

“Psoriasis is a skin disease that causes red, itchy scaly patches, most commonly on the knees, elbows, trunk and scalp. 

Psoriasis is a common, long-term (chronic) disease with no cure. It tends to go through cycles, flaring for a few weeks or months, then subsiding for a while or going into remission. Treatments are available to help you manage symptoms. And you can incorporate lifestyle habits and coping strategies to help you live better with psoriasis.” 

Now you can see why people might be lax to mention they have psoriasis. It almost appears as if you hadn’t been taking care of your personal hygiene, and no one enjoys looking at those sores. My father had it in large, constant patches, but I grew up seeing it on him and never questioned what it was or how he got it. Maybe that’s why I’m so open about having it myself. 

Oh, yes, latent. That just means it’s there, but it hasn’t made itself known yet. 

I went to WebMD for an explanation of the symptoms of psoriasis. 

“Plaques of red skin, often covered with silver-colored scales. These plaques may be itchy and painful, and they sometimes crack and bleed. In severe cases, the plaques will grow and merge, covering large areas. 

Disorders of the fingernails and toenails, including discoloration and pitting of the nails. The nails may also crumble or detach from the nail bed. 

Plaques of scales or crust on the scalp.” 

I remember a dermatologist telling me a long time ago that this skin disorder causes skin cells to produce 10 times faster than usual and asking me if I had psoriatic arthritis. I looked at him blankly. That resulted in a trip to the rheumatologist.  

Yes, that’s what I had. Arthritis.org was extremely clear about just what psoriatic arthritis [abbreviation: PsA] is: 

“Causes 

PsA (like psoriasis) is an autoimmune disease, which means the body’s immune system mistakenly attacks healthy tissue, causing inflammation and pain and resulting in damage. Researchers aren’t sure why some people develop PsA. They think it’s a combination of having certain genes, which makes them more likely to develop the disease, and being triggered by something in the environment, like an infection, stress, physical trauma or another factor.  

Symptoms: 

Skin: 

Itchy, painful red patches or a silvery white buildup of dead skin cells; most commonly on the knees, elbows and scalp, although a rash can occur anywhere on the body. It is not contagious. [Gail here: same symptoms as psoriasis] 

Joints/Spine: 

Mainly occurs in the fingers (in the joints closest to the nail), wrists, ankles and knees. Symptoms such as pain, tenderness, warmth and swelling, may affect different sides of the body (right hand and left knee). This may be referred to as peripheral arthritis. Sometimes one entire, individual finger or toe will swell up, making it painful and hard to bend. This is referred to as dactylitis. Pain and stiffness in the low back, buttock can also occur. Sometimes the neck and hips are affected and this may be referred to as spondylitis or axial arthritis.  

Nails: 

Cracking, pitting, white spots and lifting from the nail bed can occur. This may be referred to as nail disease. 

Enthesis (plural, entheses): 

Inflammation and swelling of one or more entheses, which are the places in the body where a tendon or ligament connects with a bone. Common spots include at the back of the heel and the bottom of the foot. This is called enthesitis.  
 
Many people with psoriatic arthritis get very tired (fatigue) and some may have a low-grade fever. Symptoms may come and go. A period of increased inflammation and worsening of other symptoms is called a flare. A flare can last for days or months.”   

And now for the biggie- What does any of this have to do with CKD? 

“’Psoriasis is an autoimmune disease of the skin that causes inflammation throughout the entire body,’ says Dr. Aamir Memon, nephrologist on staff at Advocate Sherman Hospital in Elgin, Ill. ‘When you have an autoimmune disease, you have antibodies in your blood, which can deposit anywhere in the body, such as your heart and kidneys. The increased inflammation increases the risk of atherosclerosis (hardening of the arteries) and organ damage.’ 

According to Dr. Memon, many patients with moderate to severe psoriasis take medications like Cyclosporine or Methotrexate as treatment. However, side effects from these medications include kidney problems. 

‘Since psoriasis has effects on the kidneys, it would intuitively make sense to control the inflammation to prevent further worsening of the kidneys,’ Dr Memon says. ‘Further studies are needed to evaluate if that is the case and as to what medications are best to decrease inflammation and prevent or halt kidney disease.’” 

Thank you to health enews at Advocate Aurora Health for the above information. This is a new site for me, so allow me to introduce you to them via their website: 

“health enews is the Midwest’s go-to source for timely, patient-centered and credible health news and information. Our goal is to provide readers with relevant and engaging articles and stories as part of our commitment to building healthy and informed communities across Illinois, Wisconsin and beyond. 

health enews is produced by a team of seasoned journalists and public affairs professionals from across Advocate Aurora Health.” 

From my 11 years of blogging about CKD, I’m beginning to accept that it is all connected. What happens to one part of the body does, indeed, affect the other parts of the body. Now you know how CKD and psoriasis are related, in case you’d ever wondered. 

You may have noticed there are no URLs in the blogs lately. Press control and click on the name of the organization instead. They are linked to the articles mentioned.

Until next week, 

Keep living your life!  

One Thing is Not Like the Other

I’d always thought that albuminuria and proteinuria were one and the same since the words are often use interchangeably. Guess who was wrong. While ‘uria,’ means:  

“a combining form with the meanings ‘presence in the urine’ of that specified by the initial element (albuminuria; pyuria), ‘condition of the urinary tract,’ ‘tendency to urinate as specified (polyuria).’’ 

according to Dictionary.com at https://www.dictionary.com/browse/-uria, albumin and protein are two different substances. 

I know they are closely related, but yet… still not the same. Let’s take a look at albumin: 

“Your liver makes albumin. Albumin carries substances such as hormones, medicines, and enzymes throughout your body.” 

Thank you to University of Rochester’s Medical Center’s Health Encyclopedia at bit.ly/3agVUO8 for this information. 

Wait a minute, the liver? I thought we were dealing with the kidneys. Let me think a minute. I know: we’ll go to the National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Disease. This is what I found at bit.ly/3pDfmer

“Albuminuria is a sign of kidney disease and means that you have too much albumin in your urine. Albumin is a protein found in the blood. A healthy kidney doesn’t let albumin pass from the blood into the urine. A damaged kidney lets some albumin pass into the urine. The less albumin in your urine, the better.” 

Oh, so the albumin itself doesn’t harm the kidneys, but is a sign of kidney disease. Got it. But it’s a protein. Let’s take a look at the protein part of proteinuria and see if we can figure this out. 

In What Is It and How Did I Get It? Early Stage Kidney Disease, I defined protein as: 

“Amino acids arranged in chains joined by peptide bonds to form a compound, important because some proteins are hormones, enzymes and antibodies.”   

Look at that: hormones and enzymes are mentioned in both definitions. It would make sense to define these two words now. According to my first book on Chronic Kidney Disease, 

“Hormones: Gland produced chemicals that trigger tissues to do whatever their particular job is.” 

I need some examples. Hormone.org has an extensive list.  Some hormones you might recognize are: 

  • Adrenaline 
  • Cortisol 
  • Erythropoietin 
  • Estrogen 
  • Glucagon 
  • Insulin 
  • Melatonin 
  • Oxytocin 
  • Serotonin 
  • Testosterone 
  • Vitamin D 

What about enzymes? The Merriam Webster Dictionary can help us out here. 

“any of numerous complex proteins that are produced by living cells and catalyze specific biochemical reactions at body temperatures” 

I don’t know about you, but I’m better with examples. I took a short list from MedicalNewsToday: 

  • Lipases 
  • Amylase 
  • Lactase 

These terms may look familiar from your quarterly blood tests. 

I still don’t get it. If albumin is a protein, why isn’t it considered proteinuria? MDEdge, a new site for me, but one that seems credible, explains: 

“Proteinuria and albuminuria are not the same thing. Proteinuria indicates an elevated presence of protein in the urine (normal excretion should be < 150 mg/d), while albuminuria is defined as an ‘abnormal loss of albumin in the urine.’…. Albumin is a type of plasma protein normally found in the urine in very small quantities. Albuminuria is a very common (though not universal) finding in CKD patients; is the earliest indicator of glomerular diseases, such as diabetic glomerulosclerosis; and is typically present even before a decrease in the glomerular filtration rate (GFR) or a rise in the serum creatinine…. 

Albuminuria, without or with a reduction in estimated GFR (eGFR), lasting > 3 months is considered a marker of kidney damage. There are 3 categories of persistent albuminuria…. Staging of CKD depends on both the eGFR and the albuminuria category; the results affect treatment considerations.” 

The important part to remember is that both are indicators of Chronic Kidney Disease. 

Switch of topics here. Remember KidneyX? That’s, 

“The Kidney Innovation Accelerator (KidneyX), a public-private partnership between the U.S. Department of Health and Human Services (HHS) and the American Society of Nephrology (ASN), is accelerating innovation in the prevention, diagnosis, and treatment of kidney diseases.”   

Well, they have an announcement for you: 

“The U.S. Department of Health and Human Services (HHS) and the American Society of Nephrology (ASN) announced the eight winners of the KidneyX COVID-19 Kidney Care Challenge Round 1. The $300,000 challenge has identified solutions that could reduce the transmission of coronavirus among people with kidney disease and/or reduce the risk of kidney damage among people who contract the virus. 

‘We congratulate the Round 1 winners who have highlighted approaches to patient monitoring, patient education, and vaccine distribution,’ said HHS Acting Assistant Secretary for Health Rear Admiral Felicia Collins, MD, MPH. ‘We look forward to the subsequent round of rapid-response innovation that supports COVID-19 risk reduction in kidney patients and health professionals during the pandemic.’ 

Each winner will receive $20,000 in recognition of their solution…. The KidneyX Round 2 winners will be announced in February, 2021. 

COVID-19 Kidney Care Challenge Round 1 Winners 

The following submissions were selected as winners of the COVID-19 Kidney Care Challenge Round 1: 

  • 9 Remote Monitoring Platform to Reduce COVID-19 Risk for Hemodialysis Patients 
  • Free E-Learning Platform with CKD and COVID-19 Patient Education 
  • Immediate Rooming for Patients 
  • Canopy: the Next Generation, Reusable Respirator 
  • Characterizing and Targeting Vaccine Hesitancy Among End-Stage Kidney Disease (ESKD) Patients 
  • COVID-19 in Translation: Making Patient Education Accessible to Minorities 
  • The ‘Good Humoral’ Immunity Truck and Freezer Project 
  • Development of Telemedicine-Enhanced Peritoneal Dialysis Training Protocols During COVID-1″ 

Did you know that patients were involved in these projects? 

We’ve passed a sort of milestone with SlowItDownCKD: this is the 601st blog. If there were no Covid-19, I would invite you all to my house for a Renal Diet Bar-B-Q. We know that’s not going to happen any time soon, so – please – have a special meal at your home with those you love. Wear your masks, keep six feet apart, wash your hands often, keep it to a very small gathering of those who are in your pod (Our pod is very small, just Bear and me.), but have a good time anyway. 

Until next week, 

Keep living your life! 

Mg or Magnesium to You and Me

We usually think of Mg (mg) as the abbreviation for milligrams. Lately, I’ve been hearing a lot about Mg as the symbol for magnesium. In fact, a friend all the way across the country in Florida sent me an article about it from her local town paper. That got me to thinking. I haven’t written about magnesium in over three years. Has anything new been uncovered about this particular electrolyte? But first we need to know what I wrote about it in SlowItDownCKD 2017.  

“The medical dictionary part of The Free Dictionary by Farlex at http://medical-dictionary.thefreedictionary.com/magnesium tells us: 

‘An alkaline earth element (atomic number 12; atomic weight 24.3) which is an essential mineral required for bone and tooth formation, nerve conduction and muscle contraction; it is required by many enzymes involved in carbohydrate, protein and nucleic acid metabolism. Magnesium is present in almonds, apples, dairy products, corn, figs, fresh leafy greens, legumes, nuts, seafood, seeds, soybeans, wheat germ and whole grains. Magnesium may be useful in treating anxiety, asthma and cardiovascular disease; it is thought to prevent blood clots, raise HDL-cholesterol, lower LDL-cholesterol, reduce arrhythmias and blood pressure, and to help with depression, fatigue, hyperactivity and migraines.’ 

All this by an electrolyte that constitutes only 1% of extra cellular fluid? I’m beginning to suspect that magnesium is the under explained electrolyte. 

All right then, what happens if you have too little magnesium?

The U.S. Dept. of Health & Human Services of the National Institutes of Health at https://ods.od.nih.gov/factsheets/Magnesium-HealthProfessional/ lays it out for us: 

‘Early signs of magnesium deficiency include loss of appetite, nausea, vomiting, fatigue, and weakness. As magnesium deficiency worsens, numbness, tingling, muscle contractions and cramps, seizures, personality changes, abnormal heart rhythms, and coronary spasms can occur …. Severe magnesium deficiency can result in hypocalcemia or hypokalemia (low serum calcium or potassium levels, respectively) because mineral homeostasis is disrupted….’ 

Well, who’s at risk for magnesium deficiency? The same source tells us: 

‘Magnesium inadequacy can occur when intakes fall below the RDA [Gail here today: RDA is the Recommended Dietary Allowances] but are above the amount required to prevent overt deficiency. The following groups are more likely than others to be at risk of magnesium inadequacy because they typically consume insufficient amounts or they have medical conditions (or take medications) that reduce magnesium absorption from the gut or increase losses from the body. 

People with gastrointestinal diseases 
The chronic diarrhea and fat malabsorption resulting from Crohn’s disease, gluten-sensitive enteropathy (celiac disease), and regional enteritis can lead to magnesium depletion over time …. Resection or bypass of the small intestine, especially the ileum, typically leads to malabsorption and magnesium loss …. 

People with type 2 diabetes [Gail again today: That’s me.] 
Magnesium deficits and increased urinary magnesium excretion can occur in people with insulin resistance and/or type 2 diabetes…. The magnesium loss appears to be secondary to higher concentrations of glucose in the kidney that increase urine output …. 

People with alcohol dependence 
Magnesium deficiency is common in people with chronic alcoholism…. In these individuals, poor dietary intake and nutritional status; gastrointestinal problems, including vomiting, diarrhea, and steatorrhea (fatty stools) resulting from pancreatitis; renal dysfunction with excess excretion of magnesium into the urine; phosphate depletion; vitamin D deficiency; acute alcoholic ketoacidosis; and hyperaldosteronism secondary to liver disease can all contribute to decreased magnesium status …. 

Older adults 
Older adults have lower dietary intakes of magnesium than younger adults …. In addition, magnesium absorption from the gut decreases and renal magnesium excretion increases with age …. Older adults are also more likely to have chronic diseases or take medications that alter magnesium status, which can increase their risk of magnesium depletion ….’” 

Okay, that was then. Let’s see if there’s more news now.  Oh, look at that! I found lots of goodies at https://ods.od.nih.gov/factsheets/Magnesium-HealthProfessional/ which is one of the same sites I used in 2017. I suggest you check this site for even more information about magnesium and your health. 

Table 1: Recommended Dietary Allowances (RDAs) for Magnesium  

Age Male Female Pregnancy Lactation 
Birth to 6 months 30 mg* 30 mg*   
7–12 months 75 mg* 75 mg*   
1–3 years 80 mg 80 mg   
4–8 years 130 mg 130 mg   
9–13 years 240 mg 240 mg   
14–18 years 410 mg 360 mg 400 mg 360 mg 
19–30 years 400 mg 310 mg 350 mg 310 mg 
31–50 years 420 mg 320 mg 360 mg 320 mg 
51+ years 420 mg 320 mg   

*Adequate Intake (AI) 
 

Table 2: Selected Food Sources of Magnesium  

Food Milligrams 
(mg) per 
serving 
Percent 
DV* 
Pumpkin seeds, roasted, 1 ounce 156 37 
Chia seeds, 1 ounce 111 26 
Almonds, dry roasted, 1 ounce 80 19 
Spinach, boiled, ½ cup 78 19 
Cashews, dry roasted, 1 ounce 74 18 
Peanuts, oil roasted, ¼ cup 63 15 
Cereal, shredded wheat, 2 large biscuits 61 15 
Soymilk, plain or vanilla, 1 cup 61 15 
Black beans, cooked, ½ cup 60 14 
Edamame, shelled, cooked, ½ cup 50 12 
Peanut butter, smooth, 2 tablespoons 49 12 
Potato, baked with skin, 3.5 ounces 43 10 
Rice, brown, cooked, ½ cup 42 10 
Yogurt, plain, low fat, 8 ounces 42 10 
Breakfast cereals, fortified with 10% of the DV for magnesium, 1 serving 42 10 
Oatmeal, instant, 1 packet 36 
Kidney beans, canned, ½ cup 35 
Banana, 1 medium 32 
Salmon, Atlantic, farmed, cooked, 3 ounces 26 
Milk, 1 cup 24–27 
Halibut, cooked, 3 ounces 24 
Raisins, ½ cup 23 
Bread, whole wheat, 1 slice 23 
Avocado, cubed, ½ cup 22 
Chicken breast, roasted, 3 ounces 22 
Beef, ground, 90% lean, pan broiled, 3 ounces 20 
Broccoli, chopped and cooked, ½ cup 12 
Rice, white, cooked, ½ cup 10 
Apple, 1 medium 
Carrot, raw, 1 medium 2” 

As mentioned in my earlier blog on magnesium: 

“Quick, go check your lab results. You’ll notice there’s no magnesium level. If you’d like your magnesium tested, you or your doctor need to order a specific test for that. Some labs will allow you to order your own magnesium test; others will require a doctor’s orders.” 

Until next week, 

Keep living your life! 

How Rare is This?

I have been hearing about so many different kinds of kidney disease that I’d forgotten which I’d written about. UMOD nephropathy is one that has kept coming up this past week or so. That got me to thinking… yep, I did write about it once before. It seems I had trouble getting any information at that time. Let’s try again. 

To start, here is some of the information about the disease that I included in SlowItDownCKD 2019. 

This is what the U.S. National Library of Medicine at bit.ly/3sykq5O had to say: 

‘Many individuals with uromodulin-associated kidney disease develop high blood levels of a waste product called uric acid. Normally, the kidneys remove uric acid from the blood and transfer it to urine. In this condition, the kidneys are unable to remove uric acid from the blood effectively. A buildup of uric acid can cause gout, which is a form of arthritis resulting from uric acid crystals in the joints. The signs and symptoms of gout may appear as early as a person’s teens in uromodulin-associated kidney disease. 

Uromodulin-associated kidney disease causes slowly progressive kidney disease, with the signs and symptoms usually beginning during the teenage years. The kidneys become less able to filter fluids and waste products from the body as this condition progresses, resulting in kidney failure. Individuals with uromodulin-associated kidney disease typically require either dialysis to remove wastes from the blood or a kidney transplant between the ages of 30 and 70. Occasionally, affected individuals are found to have small kidneys or kidney cysts (medullary cysts).’” 

By the way, the U.S. National Library of Medicine is part of the National Institutes of Health. 

I suspected I could find more information since almost two years have passed and I did. The Genetic and Rare Diseases Information Center (GARD), which is part of the National Center for Advancing Translational Sciences which, in turn, is part of the National Institutes of Health (just as the U.S. National Library of Medicine is) at Bit.ly/35KOalW offered the following:   

Autosomal dominant tubulointerstitial kidney disease due to UMOD mutations (ADTKD–UMOD) is an inherited disorder that causes a gradual loss of kidney function that eventually leads to the need for kidney transplantation or dialysis between the ages of 30 and 70. Patients with ADTKD-UMOD have high blood levels of uric acid before kidney failure develops, and some affected individuals may develop gout. Gout is a form of arthritis (inflammation) that occurs often in the big toe, ankle, knee, or other joints…. ADTKD-UMOD is caused by a mistake (mutation) in the UMOD gene, which leads to the build-up of the altered uromodulin protein in the tubules [Gail here: These are small tubes in your kidneys.] the kidney, leading to slow loss of kidney function. ADTKD-UMOD is inherited in a dominant pattern in families. It is diagnosed based on the symptoms, laboratory testing, family history and genetic testing. Many of the symptoms of ADTKD-UMOD can be treated with medication. For patients whose kidney function worsens to end-stage kidney disease, kidney transplant and dialysis can be used. The long-term outlook for people with ADTKD-UMOD is good, though patients may require dialysis or kidney transplantation between the ages of 30 and 70….” 

I was having a bit of trouble with the different names of the disease, so I turned to the National Center for Biotechnology Information (NCBI) at https://www.ncbi.nlm.nih.gov/books/NBK1356/ for clarification: 

“Autosomal dominant tubulointerstitial kidney disease caused by UMOD pathogenic variants (ADTKD-UMOD) was previously known as familial juvenile hyperuricemic nephropathy type 1 (FJHN1), medullary cystic kidney disease type 2 (MCKD2), and UMOD-associated kidney disease (or uromodulin-associated kidney disease)” 

The NCBI is ultimately also part of (surprise!) the National Institutes of Health. 

Well, that helped but you may also need this definition found in What Is It and How Did I Get It? Early Stage Chronic Kidney Disease’s Glossary: 

Nephropathy: Kidney disease.” 

Hmmm, come to think of it, we could use a few more definitions. Thank you to Medline Plus for the definitions: 

Uremic acid: Uric acid is a chemical created when the body breaks down substances called purines. Purines are normally produced in the body and are also found in some foods and drinks. Foods with high content of purines include liver, anchovies, mackerel, dried beans and peas, and beer. 

UMOD gene: The UMOD gene provides instructions for making a protein called uromodulin. This protein is produced by the kidneys and then excreted from the body in urine. The function of uromodulin remains unclear, although it is known to be the most abundant protein in the urine of healthy individuals. Researchers have suggested that uromodulin may protect against urinary tract infections. It may also help control the amount of water in urine. 

This is quite a bit of information, but we still need the symptoms? According to Wake Forest Baptist Health at bit.ly/3oRN7s8

“There are three common features of this disease: 

Patients develop chronic kidney failure with loss of kidney function beginning in the teenage years and progressing to the need for dialysis or kidney transplantation at an age between 30 and 70 years. Patients have few or no symptoms of kidney disease when they are diagnosed. 

Usually, affected individuals are found to have some loss of kidney function when they undergo blood testing by their doctor as part of a general health screening. A blood test called the serum creatinine level is performed. If the blood creatinine level is above 1, this is usually abnormal and means the kidney is not removing the creatinine from the blood well enough. …. Frequently the doctor does not know why the serum creatinine level is high. Even if a kidney biopsy (the removal of a small piece of kidney tissue) is performed, a correct diagnosis is frequently not made. 

The patient has gout or some member of the family has a history of gout …. Affected individuals have high blood uric acid levels, and this leads to gout. Every affected individual in the family may not have gout, but there are usually at least one or two people in the family who have gout. Gout frequently involves the big toe, the foot, or the knee. The big toe will become extremely tender, and even placing a sheet on the toe will cause pain. In this condition, gout occurs in the late teenage years in both men and women. (In contrast, gout developing in the normal adult population tends to occur in overweight men in their 30’s to 50’s). Family members may develop bumps on their joints called tophi that are deposits of uric acid. 

The disease is likely to be inherited. If a person has the disease, their children have a 1 out of 2 (50%) chance of having the disease. The disease does not skip a generation, though a parent may be less severely affected than their child, and may not have gout or other signs of kidney disease for some time. Therefore, there is usually a strong family history of the condition.” 

Unfortunately, there is no cure for this rare disease – there are medications available to treat the symptoms. Only 400 people worldwide suffer from UMOD Nephropathy. 

Until next week, 

Keep living your life! 

It Won’t Necessarily Get You High

About a million years ago, really in the 60s, I attended Hunter College of the City University of New York. Since it was located on Lexington Avenue and 68th Street, we had no campus. What we did have was a high raise building with what seemed to be to be huge elevators. They always smelled so sweet despite the number of bodies crammed in during the change of classes. Being an innocent, I couldn’t figure out why. 

One of my brothers was in the Air Force. When he came home on leave, I told him about this. He laughed. Being more worldly, he explained to me about cannabis. I wasn’t sure I believed him; that’s how innocent I was. Ah, but I realized I had noticed the same odor at parties I’d been invited to. 

Years later, a reader was offered medical marijuana and wanted to know if it would make him high. It wouldn’t. He chose to do without it then. 

When I had cancer, I was offered medical marijuana to replace the opioids I took after surgery. By this time, five decades after my college experience (or lack thereof), I was more than willing. Except… my oncologist explained that it would exacerbate the constipation I was enduring from the drugs I was already taking. I was already uncomfortable enough, so I decided against it. 

So, what is this cannabis of which I write? Surprise! Instead of my favorite dictionary, we’ll be using the Oxford Languages since it is more specific: 

“a tall plant with a stiff upright stem, divided serrated leaves, and glandular hairs. It is used to produce hemp fiber and as a drug. 

a dried preparation of the flowering tops or other parts of the cannabis plant, or a resinous extract of it ( cannabis resin), smoked or consumed, generally illegally, as a psychoactive (mind-altering) drug.” 

Hmmm, however does this make us high?  According to LiveScience at https://www.livescience.com/how-cannabis-high-works.html,  

“‘When a person smokes or inhales cannabis, THC [Gail here: THC is tetrahydrocannabinol, the part of cannabis that gives you a high.] ‘goes into your lungs and gets absorbed … into the blood,’ according to Daniele Piomelli, a professor of anatomy & neurobiology, biological chemistry, and pharmacology at the University of California, Irvine School of Medicine. Edibles take [sic] slightly longer trip through the liver, where enzymes transform THC into a different compound that takes a bit longer to have an effect on people’s perception of reality.”   

Wait a minute… the liver? I’m dealing with kidneys here. 

As reported on Healio at http://bit.ly/39j7WpD , Lisa Miller Hedin, BSN, RN, mentioned the following during her speech at the American Nephrology Nurses Association National Symposium last September. By the way, “Miller Hedin, the founder and CEO of the Medical Cannabis Training Academy, has been involved for 25 years in nephrology nursing and has spent the last 5 years researching cannabis treatment options.” 

“Cannabis is mostly eliminated by the liver and excreted into stool, Miller Hedin said. ‘Very little is eliminated by kidneys or dialysis.’ Cannabis is lipid soluble and can stay in a patient’s system for 80 days, she said.” 

Well, if a bit of it “is eliminated by kidneys or dialysis,” why are Chronic Kidney Disease patients using it at all? 

The nephrologist’s guide to cannabis and cannabinoids by Rein, Joshua L. Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA at http://bit.ly/39mfA2R gave me more insight.  

“Cannabis (marijuana, weed, pot, ganja, Mary Jane…) is the most commonly used federally illicit drug in the United States. As of December 2019, 33 states and the District of Columbia have medical cannabis programs. Eleven states and the District of Columbia have legalized recreational use. Several countries worldwide have legalized recreational use whereas many others have medical cannabis and decriminalization laws. The prevalence of cannabis use more than doubled between 2001 and 2013 in the United States… particularly among people over the age of 50 and even more so among those over 65 years …. These age groups are enriched with chronic illness including chronic kidney disease (CKD) that is associated with excess morbidity and mortality ….” 

Read that last line again. This time I did go to my favorite dictionary, the Merriam-Webster at https://www.merriam-webster.com/dictionary/morbidity for a specific definition – or definitions in this case – of morbidity, 

“1: the quality or state of being morbid especially: an attitude, quality, or state of mind marked by excessive gloom…  

2: a diseased state or symptom: ill health 

3: the incidence of disease: the rate of illness (as in a specified population or group) 
    also: the incidence of complications or undesirable side effects following surgery or medical                        treatment” 

I get it. We have pain. Cannabis can alleviate it without the use of opioids. But don’t necessarily expect to get high.     

Dr. Peter Grinspoon tells us via Harvard Medical School’s Harvard Health Publishing at  https://www.health.harvard.edu/blog/medical-marijuana-2018011513085,   

“Least controversial is the extract from the hemp plant known as CBD (which stands for cannabidiol) because this component of marijuana has little, if any, intoxicating properties. Marijuana itself has more than 100 active components. THC (which stands for tetrahydrocannabinol) is the chemical that causes the ‘high’ that goes along with marijuana consumption. CBD-dominant strains have little or no THC, so patients report very little if any alteration in consciousness.” 

Healthline (Remember them?) at https://www.healthline.com/health/does-cbd-get-you-high#thc seems to have the definitive word on this: 

“CBD can have several positive effects. Some of these research-backed uses of CBD even suggest it may help you feel relaxed. That can feel a bit like a high, though it’s not intoxicating…. 

Research suggests CBD is beneficial for relieving symptoms of anxiety and depression. It might also ease inflammation and pain….  

The World Health Organization says CBD is safe. However, more research is still needed to understand the full spectrum of effects and possible uses. 

Despite general acceptance, some people may experience some side effects when they take CBD, especially at high concentrations. These side effects can include: 

diarrhea 

mild nausea 

dizziness 

excessive fatigue 

dry mouth 

If you take any prescription medications, talk with your doctor before using CBD. Some medicines may be less beneficial because of CBD. They could also interact and cause unintended side effects.” 

Reminder – cannabis is not legal in all states. 

Until next week, 

Keep living your life! 

A New Year, New Kidney Disease Information

Happy New Year! Or, at least, that’s what I’m hoping for. I fervently believe the more you know, the better you can handle whatever’s happening in your world. That’s why, today, I’m exploring yet another term pertaining to kidney disease that I hadn’t been aware of. Oh my, how many, many types of kidney disease am I (and possibly you) unaware of?  

This one is membranous glomerulonephritis. I sort of-maybe-suspected what it might be, but I wanted to know for sure so I turned to Healthline – who bestowed a couple of awards on this blog a few years ago – at https://www.healthline.com/health/membranous-nephropathy for something more in the way of a definition. 

“Your kidneys are made up of a number of different structures that aid in the removal of wastes from your blood and the formation of urine. Glomerulonephritis (GN) is a condition in which changes in the structures of your kidney can cause swelling and inflammation. 

Membranous glomerulonephritis (MGN) is a specific type of GN. MGN develops when inflammation of your kidney structures causes problems with the functioning of your kidney. MGN is known by other names, including extramembranous glomerulonephritis, membranous nephropathy, and nephritis.” 

It’s hard to know where to start in exploring this disease. Let’s take the easy way and start with a definition of nephritis from… ta da, you guessed it – my all-time favorite dictionary, the Merriam Webster at https://www.merriam-webster.com/dictionary/nephritis.  

“acute or chronic inflammation of the kidney caused by infection, degenerative process, or vascular disease” 

I’m going back to the beginning of my blog journey to What Is It and How Did I Get It? Early Stage Chronic Kidney Disease for the following definitions. 

“Acute: Extremely painful, severe or serious, quick onset, of short duration; the opposite of chronic. 

 Chronic: Long term; the opposite of acute.” 

By the way, you can click on the title of the book if you’re interested in purchasing it from Amazon. 

So, basically, nephritis means a kidney problem. But membranous glomerulonephritis is something more specific in that it is a kind of GN or glomerulonephritis. Back to the dictionary for the definition of glomerulonephritis: 

“acute or chronic nephritis that involves inflammation of the capillaries of the renal glomeruli, has various causes (such as streptococcal infection, lupus, or vasculitis) or may be of unknown cause, and is marked especially by blood or protein in the urine and by edema, and if untreated may lead to kidney failure” 

Ah, so now we know what part of the kidneys are involved. Do you remember what the glomeruli are? Just in case you don’t, here’s how ‘s Lexicon at https://www.lexico.com/en/definition/glomerulus  defines this plural noun: 

“a cluster of nerve endings, spores, or small blood vessels, in particular a cluster of capillaries around the end of a kidney tubule, where waste products are filtered from the blood.” 

Now we’re getting somewhere. Let’s keep digging. Membranous glomerulonephritis is a specific GN. I went directly to MedlinePlus, which is part of the National Institutes of Health, which in turn is part of The U.S. National Library of Medicine at https://medlineplus.gov/ency/article/000472.htm

“Membranous nephropathy is caused by the thickening of a part of the glomerular basement membrane. The glomerular basement membrane is a part of the kidneys that helps filter waste and extra fluid from the blood. The exact reason for this thickening is not known. 

The thickened glomerular membrane does not work normally. As a result, large amounts of protein are lost in the urine. 

This condition is one of the most common causes of nephrotic syndrome. This is a group of symptoms that include protein in the urine, low blood protein level, high cholesterol levels, high triglyceride levels, and swelling. Membranous nephropathy may be a primary kidney disease, or it may be associated with other conditions. 

The following increase your risk for this condition: 

Cancers, especially lung and colon cancer 

Exposure to toxins, including gold and mercury 

Infections, including hepatitis B, malaria, syphilis, and endocarditis 

Medicines, including penicillamine, trimethadione, and skin-lightening creams 

Systemic lupus erythematosus, rheumatoid arthritis, Graves disease, and other autoimmune disorders 

The disorder occurs at any age, but is more common after age 40.” 

Being only a bit more than a year out from cancer, I was getting nervous so I went to the National Kidney Foundation at https://www.kidney.org/atoz/content/membranous-nephropathy-mn for a list of symptoms. 

“Swelling in body parts like your legs, ankles and around your eyes (called edema) 

Weight gain 

Fatigue 

Foaming of the urine caused by high protein levels in the urine (called proteinuria) 

High fat levels in the blood (high cholesterol) 

Low levels of protein in the blood” 

These symptoms struck me as so common that I wanted to know just how usual membranous glomerulonephritis was. After checking numerous sites, the consensus I found was that this is not a common disease. Thank goodness! 

Even though it’s not common, we still might want to know what to do if we were diagnosed with membranous glomerulonephritis, especially since I discovered that this may be considered an autoimmune disease. This is how the Mayo Clinic suggested the disease be treated: 

“Treatment of membranous nephropathy [Gail here: That’s a synonym for membranous glomerulonephritis.] focuses on addressing the cause of your disease and relieving your symptoms. There is no certain cure. 

However, up to three out of 10 people with membranous nephropathy have their symptoms completely disappear (remission) after five years without any treatment. About 25 to 40 percent have a partial remission. 

In cases where membranous nephropathy is caused by a medication or another disease — such as cancer — stopping the medication or controlling the other disease usually improves the condition.” 

There is much more detailed treatment information on their website at mayoclinic.in/354QFPU.    

That is a bit more reassuring. Thank you to all the readers who use terms I hadn’t heard of before and/or ask questions about topics that are new to me. May this year be kinder to us than the last one. 

Until next week, 

Keep living your life! 

Learning Every Day

 Chronic Kidney Disease is all over my world. You know when you have your ears open for a certain term, you seem to hear it all the time? That’s what my life has been like for the last dozen years. When I noticed a comment in a Facebook kidney disease support group about Action myoclonus–renal failure (AMRF) syndrome, I was stunned. Here was yet another possible kidney disease I’d never heard of. 

As defined by MedlinePlus, a division of the National Health Institutes (which is a division of the U.S. National Library of Medicine) at http://bit.ly/2KY6EI8,  

“Action myoclonus–renal failure (AMRF) syndrome causes episodes of involuntary muscle jerking or twitching (myoclonus) and, often, kidney (renal) disease. Although the condition name refers to kidney disease, not everyone with the condition has problems with kidney function.” 

I was intrigued and wanted to know more. So, I did what I usually do when that happens. I poked around everywhere I could think of on the internet. My first hit was on The National Center for Biotechnology Information (NCBI), which is part of The U.S. National Library of Medicine at https://www.ncbi.nlm.nih.gov/books/NBK333437/

“Action myoclonus – renal failure (AMRF) syndrome typically comprises a continuum of two major (and ultimately fatal) manifestations: progressive myoclonic epilepsy (PME) and renal failure; however, in some instances, the kidneys are not involved. Neurologic manifestations can appear before, simultaneously, or after the renal manifestations. Disease manifestations are usually evident in the late teens or early twenties. In the rare instances in which renal manifestations precede neurologic findings, onset is usually in late childhood / early adolescence but can range to the fifth or sixth decade.” 

Uh-oh, epilepsy. One of my children has that. Luckily for her, she doesn’t have CKD. But we still need more information… or, at least, I do. For instance, how does the illness progress? 

Rare Disease InfoHub at http://bit.ly/37Qgo0h answered this particular question. 

“The movement problems associated with AMRF syndrome typically begin with involuntary rhythmic shaking (tremor) in the fingers and hands that occurs at rest and is most noticeable when trying to make small movements, such as writing. Over time, tremors can affect other parts of the body, such as the head, torso, legs, and tongue. Eventually, the tremors worsen to become myoclonic jerks, which can be triggered by voluntary movements or the intention to move (action myoclonus). These myoclonic jerks typically occur in the torso; upper and lower limbs; and face, particularly the muscles around the mouth and the eyelids. Anxiety, excitement, stress, or extreme tiredness (fatigue) can worsen the myoclonus. Some affected individuals develop seizures, a loss of sensation and weakness in the limbs (peripheral neuropathy), or hearing loss caused by abnormalities in the inner ear (sensorineural hearing loss). Severe seizures or myoclonus can be life-threatening.” 

But we haven’t looked at the kidneys yet. How are they involved in those who develop kidney problems from this rare disease? Let’s go back to MedlinePlus to see what we can find. Don’t be surprised that the answer is fairly general: 

“When kidney problems occur, an early sign is excess protein in the urine (proteinuria). Kidney function worsens over time, until the kidneys are no longer able to filter fluids and waste products from the body effectively (end-stage renal disease).” 

Do you remember what proteinuria is? Here’s a reminder from my first CKD book – What Is It and How Did I Get It? Early Stage Chronic Kidney Disease – in case you’ve forgotten: 

“Protein in the urine, not a normal state of being” 

Hmmm, proteinuria is exactly what it sounds like. That got me to thinking: How does the protein get into the urine in the first place? 

“Protein gets into the urine if the kidneys aren’t working properly. Normally, glomeruli, which are tiny loops of capillaries (blood vessels) in the kidneys, filter waste products and excess water from the blood. 

Glomeruli pass these substances, but not larger proteins and blood cells, into the urine. If smaller proteins sneak through the glomeruli, tubules (long, thin, hollow tubes in the kidneys) recapture those proteins and keep them in the body. 

However, if the glomeruli or tubules are damaged, if there is a problem with the reabsorption process of the proteins, or if there is an excessive protein load, the proteins will flow into the urine.” 

Thank you to a trusted site, The Cleveland Clinic at http://cle.clinic/3nTjLZI for helping us out here.

The important point here is that proteinuria, or albumin as it is often called, prevents the substances that belong in your blood stream from fully remaining there to help you: 

“Blood contains two main kinds of proteins: albumin and globulins. Blood proteins help your body produce substances it needs to function. These substances include hormones, enzymes and antibodies. 

Usually, the amount of total protein in your blood is relatively stable.” 

I’d gone back to the reliable Cleveland Clinic for this information. 

I don’t know about you as you read today’s blog, but I found writing it exhausting. Of course, that may be due to the fact that Christmas Eve and Christmas Day have just passed. I’m not quite as vigilant as I usually am about the renal diet during certain celebrations. Considering that Bear’s Lutheran and I’m Jewish, that was a lot of celebrating. I see my exhaustion as an endorsement to get right back on the kidney diet. 

Here’s hoping your Chanukah, Christmas, Boxing Day, and Kwanza were as happy as you’d hoped under the restrictions of small group gatherings, six foot distancing, and mask wearing. We stayed home alone using the phone and Facetime to be with family.  

It was… different. But more importantly, it was safe. Keep in mind that you’re already immuno-compromised simply by having CKD. If you no longer have a spleen like me (Thanks, pancreatic cancer.), you’re even more immunocompromised. Hugs are the best, but they could be deadly for us. Stay safe. 

Until next week, 

Keep living your life! 

Baby, It’s Cold Outside. I Mean Inside.

As a diabetic, I have my feet checked and my toenails cut every nine weeks. When I was at my podiatrist’s recently, we both made mention of my slightly blue skin at the same time. I thought it was just thin skin showing the veins underneath. That’s when she mentioned a syndrome I’d heard of many times, but had never explored: Raynaud’s Syndrome, named after the Frenchman who discovered it. 

Hmmm, I wondered. Could this be related to Chronic Kidney Disease? So, of course, I looked for answers to my questions. Let’s get the basics down first… like what is it? 

Circulation Foundation at http://bit.ly/37yxSy4 answers that question.  

“Raynaud’s is a common condition where the blood supply to the extremities is interrupted or reduced. This usually affects the fingers and toes, but occasionally the nose or ears. 

Attacks are usually provoked by cold or a sudden change in temperature. During an attack the affected body part first becomes white, then turns blue as the tissues use up the oxygen and finally bright red as the arteries relax and fresh blood rushes in. 

Raynaud’s can vary in form, from very mild to severe cases – which can require treatment. 

Anyone of any age can suffer from Raynaud’s, but younger women are affected more commonly. It seems to be a change in temperature, rather than just exposure to cold that precipitates an attack, so although worse in winter, it can occur in summer too. 

Stress or anxiety can also provoke a Raynaud’s attack. Some cases of Raynaud’s are associated with some other diseases (called secondary Raynaud’s).” 

Uh, secondary Raynaud’s? What’s that? Back to the drawing board or, in this case, the researching mode. Let’s try WebMD. Bingo! 

“Secondary Raynaud’s (Raynaud’s syndrome, Raynaud’s phenomenon) happens as a result of another illness. It’s often a condition that attacks your body’s connective tissues, like lupus or rheumatoid arthritis. It’s less common, but it’s more likely to cause serious health problems. This can include things like skin sores and gangrene. These happen when cells and tissue in your extremities die from lack of blood.” 

Then, according to WebMD at http://wb.md/3h3fznI, IF I have Raynaud’s, it’s probably secondary Raynaud’s. But what about the terms Raynaud’s syndrome and Raynaud’s phenomenon in the quote above? Are they interchangeable? 

Hello, my favorite dictionary. The Merriam-Webster Medical Dictionary at http://wb.md/3h3fznI tells us that Raynaud’s phenomenon is the same as Raynaud’s syndrome: 

“the symptoms associated with Raynaud’s disease 

— called also Raynaud’s syndrome” 

Of course, that brings up another question. Symptoms are mentioned in the definition. What are the symptoms of Secondary Raynaud’s? I’ll bet the Mayo Clinic at http://mayocl.in/3pn9fur can help us out here. 

“Cold fingers or toes 

Color changes in your skin in response to cold or stress 

Numb, prickly feeling or stinging pain upon warming or stress relief 

During an attack of Raynaud’s, affected areas of your skin usually first turn white. Then, they often turn blue and feel cold and numb. As you warm and your circulation improves, the affected areas may turn red, throb, tingle or swell. 

Although Raynaud’s most commonly affects your fingers and toes, it can also affect other areas of your body, such as your nose, lips, ears and even nipples. After you warm up, the return of normal blood flow to the area can take 15 minutes.” 

I should mention here that severe cases of Secondary Raynaud’s are rare. Also, I can honestly say that I have each of these symptoms at times. As far as the cold, I figured it was just anemia. Wrong. 

We know what Secondary Raynaud’s is, what the symptoms are, and that it need not be serious, but how do you treat it? 

Wait, wait, wait. I just found this from the Merck Manual, Consumer Edition at http://bit.ly/38oZwwr

“Raynaud syndrome, a functional peripheral arterial disease, is a condition in which small arteries (arterioles), usually in the fingers or toes, narrow (constrict) more tightly than normal in response to exposure to cold.” 

It’s a PAD? Oh, excuse me, that means “peripheral arterial disease,” as mentioned above. Let’s get a definition. Back to the Merriam Webster Medical Dictionary. This time at http://bit.ly/37CdR9P:  

“damage to or dysfunction of the arteries outside the heart resulting in reduced blood flow” 

Hmmm, the podiatrist did mention spasms in the arteries at the extreme ends of my body, meaning my fingers and toes. This is all starting to make sense now. 

But we were going to see what we could find out about treatment before I made the PAD discovery. Let’s go back to that.  MedicalNewsToday at https://www.medicalnewstoday.com/articles/176713 had quite a bit of information: 

“There is no cure for Raynaud’s disease, but there are ways to manage symptoms. 

For mild forms of Raynaud’s disease, covering exposed skin before leaving the house can help. If an attack occurs, soaking the affected parts in warm, not hot, water can alleviate symptoms and prevent them from worsening. 

If stress is a factor, learning to manage stress can help. 

For moderate to severe cases, medication may be necessary. 

Alpha-1 blockers can counter the effect of norepinephrine, which constricts blood vessels. Examples include doxazosin and prazosin. 

Dihydropyridine calcium channel blockers relax the smaller blood vessels of the hands and feet. Examples include amlodipine, nifedipine, and felodipine. 

Topical nitroglycerin ointment applied to the affected area appears to relieve the symptoms by improving blood flow and cardiac output and decreasing blood pressure. 

Other vasodilators dilate the veins, easing symptoms. Examples include losartan, sildenafil (Viagra), fluoxetine (Prozac), and prostaglandin.” 

They also talk about surgery and/or chemical injections for severe cases. 

The funny thing is I live in Arizona. We have winter… sort of, but nothing drastic like snow and ice. I also take losartan for high blood pressure and to protect my kidneys. As for stress, that is present now with me just recovered from the double hernia surgery, my bother in a health care facility for Parkinson’s dementia, my husband’s Alzheimer’s and someone extremely close to my children in ICU with Covid-19 and other illnesses. (Reading this, I wonder why I’m not depressed!) 

Until next week, 

Keep living your life! 

D&C Now has Another Meaning

We usually think of a D&C as a women’s issue:  

“Dilation and curettage (D&C) is a procedure to remove tissue from inside your uterus. Doctors perform dilation and curettage to diagnose and treat certain uterine conditions — such as heavy bleeding — or to clear the uterine lining after a miscarriage or abortion.” 

Thank you to MayoClinic at https://mayocl.in/3oOzkC2 for the above explanation. 

But that’s not what I’ll be writing about today. The ‘D’ in the title stands for Dialysis and the ‘C‘ for Covid-19. Yes, Covid-19 has struck close to home for us. Someone my grown children are very close to has tested positive. He also started dialysis so recently that he hasn’t yet accepted that this is what is keeping him alive. 

Let’s get some definitions out of the way first. Take it away, Merriam-Webster Dictionary

Dialysis:  1. the separation of substances in solution by means of their unequal diffusion through semipermeable membranes 

                 2. the process of removing blood from an artery (as of a patient affected with kidney failure), purifying it by dialysis, adding vital substances, and returning it to a vein 

Covid-19: a mild to severe respiratory illness that is caused by a coronavirus (Severe acute respiratory syndrome coronavirus 2 of the genus Betacoronavirus), is transmitted chiefly by contact with infectious material (such as respiratory droplets) or with objects or surfaces contaminated by the causative virus, and is characterized especially by fever, cough, and shortness of breath and may progress to pneumonia and respiratory failure 

NOTE: While fever, cough, and shortness of breath are common symptoms of COVID-19, other symptoms may include fatigue, chills, body aches, headache, loss of taste or smell, sore throat, runny nose, nausea, vomiting, or diarrhea. 

 Here are an additional couple of definitions you may need. They’re from the glossary of What Is It and How Did I Get It? Early Stage Chronic Kidney Disease. 

Arteries: Vessels that carry blood from the heart. 

Veins: Vessels that carry blood toward the heart. 

Now what? Let’s see if we can find out how Covid-19 affects dialysis patients. The Clinical Journal of the American Society of Nephrology (CJASN) at https://cjasn.asnjournals.org/content/15/8/1087 reports the following in an August study: 

“The patients with kidney disease who appear most at risk for COVID-19 are those with a kidney transplant, due to immunosuppression, and those who undergo in-center hemodialysis treatments thrice weekly, due to inability to self-isolate. Patients with kidney disease also have other comorbidities, including hypertension, diabetes mellitus, and cardiovascular disease, that are risk factors for poor outcomes in COVID-19.” 

On December 1 of this year, the Centers for Disease Control and Prevention (CDC) cautioned those of us with chronic kidney disease, including those on dialysis: 

“Having chronic kidney disease of any stage increases your risk for severe illness from COVID-19. 

Actions to take 

Continue your medicines and your diet as directed by your healthcare provider. 

Make sure that you have at least a 30-day supply of your medicines. 

Stay in contact with your healthcare team as often as possible, especially if you have any new signs or symptoms of illness. Also reach out to them if you can’t get the medicines or foods you need. 

If you don’t have a healthcare provider, contact your nearest community health or health department. 

Have shelf-stable food choices to help you follow your kidney diet. 

If you are on dialysis: 

Contact your dialysis clinic and your healthcare provider if you feel sick or have concerns. 

Do NOT miss your treatments. 

Plan to have enough food on hand to follow the KCER 3-Day Emergency Diet for dialysis patients in case you are unable to maintain your normal treatment schedule. 

Learn more about kidney disease. 

Learn how to take care of your kidneys.” 

The KCER 3-Day Emergency Diet is not that intricate, but it is a long explanation. Click on the link to go right to the diet itself. 

We know the best way to deal with Covid-19 is prevention. I’m sure you’re tired of hearing it, but here are the ways you can hopefully do just that. This information was posted on the World Health Organization’s (WHO) website at bit.ly/3nfeMCB on December 8th of this year. 

“Maintain at least a 1-metre [Gail here: that’s 3.28 ft, so I’d be more comfortable with 2-metres.] distance between yourself and others to reduce your risk of infection when they cough, sneeze or speak. Maintain an even greater distance between yourself and others when indoors. The further away, the better. 

Make wearing a mask a normal part of being around other people. The appropriate use, storage and cleaning or disposal are essential to make masks as effective as possible. 

Here are the basics of how to wear a mask: 

Clean your hands before you put your mask on, as well as before and after you take it off, and after you touch it at any time. 

Make sure it covers both your nose, mouth and chin. 

When you take off a mask, store it in a clean plastic bag, and every day either wash it if it’s a fabric mask, or dispose of a medical mask in a trash bin. 

Don’t use masks with valves….  

How to make your environment safer 

Avoid the 3Cs: spaces that are closed, crowded or involve close contact. 

Outbreaks have been reported in restaurants, choir practices, fitness classes, nightclubs, offices and places of worship where people have gathered, often in crowded indoor settings where they talk loudly, shout, breathe heavily or sing. 

The risks of getting COVID-19 are higher in crowded and inadequately ventilated spaces where infected people spend long periods of time together in close proximity. These environments are where the virus appears to spreads by respiratory droplets or aerosols more efficiently, so taking precautions is even more important. 

Meet people outside. Outdoor gatherings are safer than indoor ones, particularly if indoor spaces are small and without outdoor air coming in…. 

Avoid crowded or indoor settings but if you can’t, then take precautions: 

Open a window. Increase the amount of ‘natural ventilation’ when indoors…. 

Wear a mask (see above for more details).  

Don’t forget the basics of good hygiene 

Regularly and thoroughly clean your hands with an alcohol-based hand rub or wash them with soap and water. This eliminates germs including viruses that may be on your hands. 

Avoid touching your eyes, nose and mouth. Hands touch many surfaces and can pick up viruses. Once contaminated, hands can transfer the virus to your eyes, nose or mouth. From there, the virus can enter your body and infect you. 

Cover your mouth and nose with your bent elbow or tissue when you cough or sneeze. Then dispose of the used tissue immediately into a closed bin and wash your hands. By following good ‘respiratory hygiene’, you protect the people around you from viruses, which cause colds, flu and COVID-19. 

Clean and disinfect surfaces frequently especially those which are regularly touched, such as door handles, faucets and phone screens.” 

This is a long, but necessary, blog. Just a bit more now. 

I’d wondered why dialysis patients are so much more at risk of Covid-19 and was surprised at how simple and common sense the reasons are. These are gathered from multiple sites that agree that shared rides, the inability to quarantine (since hemodialysis patients usually need to go to a dialysis center), and closer than six feet distancing at the centers (if that’s the case) all contribute to the susceptibility of dialysis patients to Covid-19. 

Please be safe. 

Until next week, 

Keep living your life! 

To Dye or Not

Last week, I underwent a three-month scan for cancer. I am still cancer free, so let’s get that out of the way. I’m so cancer free that I started thinking about those with kidney cancer who have scans. That’s when I started asking questions about this procedure that I’ve already undergone what seems like a million times. My questions, while answered by the technicians, of course led me to other questions. Here are the answers. 

Let’s start at the beginning. Do we use CT or CAT Scan when referring to this kind of test? According to Cincinnati Children’s Hospital Medical Center’s Blog at https://bit.ly/3lKrkjP:  

“… CAT and CT scans both mean the same type of diagnostic examination. CAT was used earlier in its history, while CT is the recent up-to-date term for convenience sake. The term CT stands for computed tomography and the term CAT stands for computed axial tomography or computerized axial tomography scan.” 

Huh? I get ‘computed,’ but what’s ‘tomography’? On to my favorite dictionary of all time. You guessed it; The Merriam-Webster Dictionary at https://www.merriam-webster.com/dictionary/tomography tells us, it’s: 

“a method of producing a three-dimensional image of the internal structures of a solid object (such as the human body or the earth) by the observation and recording of the differences in the effects on the passage of waves of energy impinging on those structures” 

Ah, that makes sense. Now what about this iodine dye that we, as Chronic Kidney Disease patients, are not supposed to have? I went to Inside Radiology at https://www.insideradiology.com.au/iodine-containing-contrast-medium/ for information. 

“Iodine-containing contrast medium (ICCM), sometimes called contrast or contrast medium, is a chemical substance used in medical X-ray imaging [Gail here: CT is a sort of X-ray.]. When injected into the body, ICCM shows what is happening inside the hollow parts of the body (like blood vessels, the stomach, bowel or even the fluid around the spinal cord) on X-ray images or pictures. When injected into a blood vessel, which can be either an artery or a vein, it not only shows the inside of the blood vessel, but it can give information about how the organs supplied by that blood vessel are working. Good examples of this are the kidneys, brain and lungs.” 

I still have my port from chemotherapy, so that was used to inject the iodine dye. Reminder, 

“A chemo port is a small, implantable reservoir with a thin silicone tube that attaches to a vein. The main advantage of this vein-access device is that chemotherapy medications can be delivered directly into the port rather than a vein, eliminating the need for needle sticks.” 

Thank you, Moffit Cancer Center, at https://moffitt.org/treatments/chemotherapy/what-is-a-chemo-port/ for this information. It’s pretty clear ports can also be used for the dye, blood draws, and infusions of any kind. For example, I’m receiving iron infusion once a week via my port. 

I know the big question here is why am I having contrast dye when it’s not recommended for CKD patients. Let’s take a closer look at that warning.

“’The historical fears of kidney injury from contrast-enhanced CT have led to unmeasured harms related to diagnostic error and diagnostic,’ explained lead author Matthew S. Davenport, MD, associate professor of radiology and urology at the University of Michigan in Ann Arbor, Michigan. ‘Modern data clarify that this perceived risk has been overstated….’” 

The above statement is from U.S. Pharmacist at https://www.uspharmacist.com/article/risk-of-contrast-media-in-reduced-kidney-function-patients-overstated

I’m comfortable with iodine contrast. First, it was clear that cancer took precedence over my kidney health, but now I’m not worried about it because of the overstatements. 

After the CT, saline was infused into my port. Wolf Medical Supply at https://bit.ly/3gjx8Q6 did a great job of explaining what this is and how it’s preformed in layman’s terms: 

“A saline flush is used to help prevent IV catheters from becoming blocked and to help remove any medication that may be left at the catheter site. 

A saline flush is a sterile mix of salt and water that is compatible with your body’s fluids and tissues. Typically, the healthcare provider will fill a syringe using a bottle of normal saline solution or use a prefilled flush syringe that’s been prepared under sterile conditions. 

To flush the IV, first, clean the IV port or hub, then connect an IV saline flush syringe to the port, slowly pull back on the syringe plunger, inject the saline solution into the IV line, and then start the medication drip. Before beginning another infusion, your provider will flush the line again.” 

We’re not done yet, though. Next came a heparin flush. Does the word ‘heparin’ sound familiar?  According to Drugs.com at https://bit.ly/3qvmGcW,   

“Heparin is an anticoagulant (blood thinner) that prevents the formation of blood clots. Heparin is used to treat and prevent blood clots caused by certain medical conditions or medical procedures. It is also used before surgery to reduce the risk of blood clots.” 

I didn’t understand why I needed heparin after a CT. WebMD at https://bit.ly/3mUeCjK explained: 

“This medication is used to keep IV catheters open and flowing freely. Heparin helps to keep blood flowing smoothly and from clotting in the catheter by making a certain natural substance in your body (anti-clotting protein) work better….” 

While I understood the CT process now, and hope that you do, too, there are warnings in place. For example,  

“Patients with kidney failure or other kidney problems should notify their doctor. In some cases, the contrast media can cause kidney failure, especially in patients with underlying kidney problems or dehydration. Patients taking the diabetes medication metformin (Glucophage), or its derivatives, who receive contrast are at increased risk of developing a condition called metabolic acidosis, or an unsafe change in blood pH, and the drug may be halted for 48 hours after the procedure.” 

The above is also from WebMD, but this time at https://www.webmd.com/drugs/2/drug-60428/heparin-lock-intravenous/details.  

I take the warning to mean speak with your nephrologist first. Although, your case may be like mine was: cancer first, then kidneys, especially if it’s kidney cancer. But we always speak with our nephrologists first, don’t we?  

Until next week, 

Keep living your life!

Feeling Nostalgic

It’s getting closer to the end of the year. Halloween and Thanksgiving have passed. Chanukah, Kwanzaa, and Christmas will be upon us sooner than we think. And then, the new year. But my nostalgia deals with the history of acknowledging and treating kidney disease. I was lucky enough to stumble across the following early history at https://hekint.org/2017/01/30/history-of-nephrology-beginnings/. It’s from Hektoen International, A Journal of Medical Humanities. I must warn you it’s a long article, but well worth the read. Enjoy: 

“History of nephrology: beginnings 

George Dunea 
Chicago, Illinois, United States 

 ….Mesopotamia 

Some of the earliest knowledge about kidney and urinary diseases comes from the cradle of Western civilization, Mesopotamia, from the cuneiform clay tablets of Akkadia, Assyria, and Babylon that contain references to urinary obstruction, stone, cysts, urethritis, stricture, and urethral discharge…. In ancient Babylon physicians made diagnoses depending on whether the urine looked like paint, wine dregs, beer, or beet juice. They treated symptoms with remedies derived from plants or minerals. They administered drugs by blowing them through a tube into the urethra, most likely also to relieve urinary obstruction, and using alcohol as an anesthetic. Much of the medical information generated in Mesopotamia was later transmitted to the Mediterranean, especially to Greece….  

Egypt 

In ancient Egypt priest-physicians have recorded many details of their patients’ symptoms on papyrus scrolls. Curiously, they cooked some of their old papyri books in oil and smeared them on their patients to relieve symptoms of dropsy or fluid retention…. They embalmed their dead, removing most of the viscera but leaving behind the kidneys and the heart. In the Ebers papyrus of 1550 BCE they refer to retention of urine, dysuria, and frequency. Hematuria, mentioned over 50 times, was probably due to schistosomiasis, then as now endemic in the valley of the Nile. Examination of mummies has led to discovery of kidney abscesses and stones, parasite ova, and congenital renal deformities. Treatments are listed in the Ebers papyrus in some 24 paragraphs under the heading: ‘Starting remedies to make disappear the retention of urine when the lower abdomen is full.’…  

Greece 

Records of urinary disorders are found in the Hippocratic Corpus, a collection of some 60 treatises that may represent the work of several medical writers. How much was written by Hippocrates himself remains uncertain. Nevertheless, Hippocrates of Cos (460–377 BCE) is regarded as the father of medicine, and many of the aphorisms attributed to him refer to diseases of the kidney: 

‘Bubbles appearing on the surface of the urine indicate disease of the kidneys and a prolonged illness.’ 
‘Colorless urine is bad.’ 
‘The sudden appearance of blood in the urine indicates that a small renal vessel has burst.’ 
‘Diseases of the kidney and of the bladder are difficult to cure in old age.’ 

Other comments concern cases where the urine was turbid or contained pus or blood, bran-like particles, or sandy sediment…. 

Aristotle, whose opinions dominated Western thought for over 2,000 years, also wrote about the kidney. From his observations on fish and birds he concluded that the kidneys were not essential to life, and from the rhesus monkey he incorrectly deduced that the right kidney was situated higher than the left. He thought the kidneys were there to anchor the blood vessels in the body, and also to secrete fluid not eliminated otherwise. He considered renal fat as the cause of cancer and of gangrene, and in De Partibus Animalium noted that ‘very often the kidneys are found to be full of stones, growths, and small abscesses.’… 

In the 3rd and 2nd century BCE other Greek physicians also made contributions, describing the prostate gland, declaring that urine was formed in the kidney, reporting on recto-vesical fistula, and performing operations. They applied pressure over the lower abdomen to relieve urinary retention, and recommended the use of poultices with soothing and diuretic properties over the kidneys…. 

Rome and Byzantium 

Physicians in Rome were often Greeks from Asia Minor who had studied in Alexandria…. Celsus (63 BCE–14 CE), though not a physician, wrote on many medical subjects, including lithotomy and the use of a bronze catheter…. In his writings, Pliny the Elder also refers to the kidney…. Areteus of Capadocia (81–138 CE), now remembered mainly for describing diabetes mellitus as the melting of the flesh into the urine, wrote about hydronephrosis, gout, renal colic, strangury, postobstructive diuresis, edema, and the anemia of renal insufficiency…. Dioscorides, also from Asia Minor and perhaps physician to emperor Nero, practiced in Rome during the first century and wrote an extensive pharmacopoeia, noting that certain poisons caused renal inflammation, and recommending enemas with ptisan or mallow for renal failure…. Galen of Pergamon (130–200 CE), physician to emperor Marcus Aurelius, referred in his extensive writings to renal cysts, breakage of the capillaries into the kidney, thrombosis, and inflammation. Called the father of experimental medicine, he ligated the ureters to prove that urine flowed from the kidneys to the bladder…. 

Among Byzantine physicians, Rufus of Ephesus in the first century CE described renal failure, abscesses, and calculi, recommending poultices of grilled cicadas as a diuretic, advising flushing the kidneys with large amounts of water, and prescribing urinating in a hot bath to relieve retention of urine. Somewhat later Oribasius (326–403), physician to emperor Julian the Apostate, wrote profusely on medical matters, summarizing the works of Galen and others in 70 books…. First to use the term ‘ureter,’ he treated dysuria and ureteral stone, did anatomical dissections, described the systemic and pulmonary circulation, discerned the existence of capillaries, and suggested that the kidneys absorbed urine from the blood stream…. 

In the 9th century Theophanes Nonus noted hematuria resulting from poisonous remedies and from the venom of serpents…. Other Byzantine physicians wrote right up to the 14th century about kidney inflammation and failure, emphasizing the changes in the appearance of the urine, developing the practice of uroscopy,… and often achieving fame as physicians to the Byzantine emperors. 

 Arabs 

The 9th and 10th centuries were a golden age for Arab medicine, in which several physicians achieved fame for their clinical acumen and perspicacious observations. Rhazes (865–925), a musician who later became a physician and was called the Galen of Islam,…described in his many clinical writings renal abscess or severe infections with pus in the urine, kidney stones, and renal failure from systemic diseases. Even more prolific was Avicenna (980–1037), poet, politician, and writer, whose works greatly influenced Western Renaissance medicine and who wrote extensively on the color, density, odor, and sediments of urine, foreshadowing the later uroscopists. Recommended treatments included inserting a bug or louse into the urethral meatus to stimulate micturition. He wrote several excellent descriptions of clinical cases, as did several other Arab authors until the 13th century…. 

There were also eminent Jewish physicians living in the Arab possessions around the Mediterranean, notably Moses Maimonides (1138–1204), born in Cordova but eventually settling down in Cairo and attending on the sultan Saladin. A renowned medieval rabbi, philosopher, astronomer, and physician, he wrote 10 treatises on medicine, including an entire chapter of aphorisms dealing with urinalysis. He discussed lower urinary tract obstruction, hesitancy, narrow stream, retention, pyuria, and hematuria. He agreed with Hippocrates that diseases of the kidney in the elderly were difficult to cure, and noted red urine in patients who probably had glomerulonephritis. In patients with blackwater fever he noted that ‘black urine and black sediment are extremely malignant and indicate serious illness. They occur in association with what resembles the death of natural resources . . . I have never seen anyone who urinated black urine who survived.’…  

Uroscopy 

Uroscopy, the naked eye examination of the urine for diagnosis, is as old as medicine itself, based on the assumption that diseases could be identified and treated following such visual inspection…. It was advocated by Hippocrates, though without much enthusiasm…. Several of the Greek physicians practiced uroscopy and helped develop a complex diagnostic model based on the theories of the four humors…. Many treatises on uroscopy were published in antiquity and later by Byzantine, Arab, and Latin physicians…. Uroscopic theory and practice reached an apogee between the 9th and 14th century in southern Italy at the medical school of Salerno, then a melting pot of different cultures…. There several masters of medicine or magistri wrote (or translated from Arabic) books on diagnostic uroscopy. One of its major exponents, Isaac Ebreus Isaac (880–940), assembled in his Guida Medicorum many of the principles of uroscopy. He was followed by Magister Maurus, according to whom fluids were separated in the body by the stomach and liver, with the generation of humors (1250 CE). Gilles de Corbeil, a Frenchman, went to Salerno, then returned to Paris and wrote Songs on Urinary Judgements, a composition in verse that remained popular until the 16th century.17 A 13th century anonymous manuscript titled De Urinis contains aphorisms such as: 

Clear urine, pale or almost green indicates pain in the stomach in males, but in women means inflammation or phlegm from the umbilicus to the throat, and thirst. 
Small volume urine which is sulphurous indicates diarrhea. 
Urine which is red with fluid beams indicates disease of the spleen. 
A red circulus means pain in the head due to blood. 
Urine of a vicious woman is quite colored, cloudy by night, and dense in the morning. 
Urine of a virgin is clear, white, light, and transparent, with very small bubbles on the surface….  

Sclerosis of the kidneys 

Hardening or sclerosis of the kidneys had been recognized as the hallmark of chronic renal failure since antiquity…. Thus Rufus of Ephesus compiled a treatise in which he noted that sclerosis of the kidneys was not painful, but might cause dropsy. He recommended rest, enemas, cupping of the loins, baths, refrigerant and sedative medicines given internally…. Aetius of Amida (502–575), court physician to emperor Justinian in Constantinople, based his Tetrabiblion largely on the works of Rufus, Hippocrates, and Galen, and also mentioned hardening of the kidneys…. Paul of Aegina (625–690), practicing in Alexandria even after the Arab conquest, also noted renal hardening and wrote in his seven books that ‘when hardness occurs in the kidneys it does not cause pain . . . but the limbs lose their strength, little urine is passed, and the whole habit resembles that of dropsical persons.’ He recommended emollients to soften the kidneys, frictions and fomentations, clysters to clear out the bowels, and diuretics such as nard, cassia, St. John’s wort pepper, sweet hay, boiled squill in wine and honey, moist alum, flakes of copper, and should all fail, ox dung dried and drunk (one spoonful every day)…. 

Also aware of sclerosis of the kidneys as a cause of illness were the Arab physicians Rhazes and Avicenna…. William of Saliceto (1210–1277) observed that hard kidneys (duritie in renibus) were difficult or even impossible to treat. He moved to Bologna in 1269 to become an outstanding teacher of medicine, and during his time taught more than 10,000 students…. He emphasized bedside instruction and wrote an extensive medical textbook, mentioning that hardness of the kidney could be the result of an abscess, an episode of high fever, or arise spontaneously. The hardness, he wrote, looks chalk-like. Its clinical signs were a reduction in urinary output, a dull pain or heaviness in the back and sides, and after a time enlargement of the belly and generalized edema…. 

Later, the Flemish physician Jan Baptiste Van Helmont (1579–1644) devoted much of his time to research, carrying out autopsies on patients who had died with gross ascites, noting that their kidneys were shrunken and hard, and concluding that the kidney was the cause of the edema …. 

Morgagni 

Giovanni Battista Morgagni (1682–1771), often regarded as the founder of pathological anatomy, made similar observations. After studying in Bologna with Valsalva, he moved to Padua, where he remained professor of theoretical medicine and anatomy for 50 years. He carried out many autopsies, correlating anatomical findings with the clinical symptoms. 

Towards the end of his career he published observations on cases he had studied over 50 years, including necropsy descriptions of diseased kidneys: solitary, asymmetrical, irregular, hardened, softened, suppuration, hydronephrosis, calculi, tumors, cysts…. Of particular interest, he described a patient who had suffered from nausea, vomiting, headache, and episodes of loss of consciousness, and who at autopsy had greatly shrunken, hard, irregularly shaped greyish kidneys. He concluded that these renal changes were the cause of the symptoms….  

Paracelsus 

Theophrastus Bombastus von Hohenheim (1493–1541), better known as Paracelsus, is perhaps the most colorful medical figure of the Renaissance. Born in Switzerland, he studied medicine in several European cities, practiced in Strasbourg and Basel, and eventually wandered through various German, Swiss, and Austrian towns. His death has often been subject of speculation, being variously attributed to murder, accident, congenital syphilis, liver failure, and also to kidney disease, as suggested by the finding of rickets in his exhumed skull in 1880…. 

Paracelsus wrote on urinalysis, proteinuria, hematuria, and gout. Particularly interested in dropsy, he described its symptoms and signs, commented on its prognosis, noted that in its advanced stages ‘the urine decreases and thickens,’ and was first to use mercury for treatment. He attempted chemical analysis of the urine, adding wine or vinegar or rennet to it and noting that it curdled and produced a precipitate. He also assessed urine by its weight, a precursor of measuring the specific gravity. He combined medicine with alchemy and astrology, and claimed to affect many cures with his Tincture of Philosophers. …  

Andreas Vesalius 

Born in Brussels, Andreas Vesalius (1514–64) studied in Paris and Padua, and on the day after graduation was appointed professor of anatomy at the University of Padua. There he carried out many dissections and became famous for his lectures and anatomical drawings. Between the ages of 24 and 27 he prepared a book of over 700 pages of anatomical illustrations, and eventually became physician to Emperor Charles V. In his famous plates he described the anatomy of the kidney, also attempting to understand its function, and concluding that urine extracted from the blood entered a cavity before being excreted into the urinary passages. His brilliantly illustrated textbook of anatomical illustrations has been reproduced for centuries….  

Marcello Malpighi 

Founder of microscopical anatomy, and professor of anatomy at Messina and later at Bologna, Marcello Malpighi (1628–94) was first to describe the renal glomerulus (Malpighian corpuscle). Using the microscope as avant-garde technology, he also studied the brain, liver, tongue, lung, and skeletal muscle, describing their architecture and postulating what their function might be. In the course of his studies of the frog’s mesentery, he discovered the presence of capillaries. In the kidney he described the pyramids of the renal medulla and the collecting ducts, and noted the opening of these ducts at the papilla. In the omentum of the porcupine he first noticed the red cells, which he interpreted as being fat globules or constituents of coagulated blood. Using a microscope with x30 magnification and sometimes with prior dye injection, he described the glomeruli, which when injected ‘turned black . . . hanging like apples from the blood vessels, which, swollen with the black fluid, look like a beautiful tree.’…” 

Many, many thanks to Dr. Dunea for what I consider fascinating history. And thank you for indulging my nostalgia. 

Until next week, 

Keep living your life! 

They’re No Laughing Matter

I may have mentioned a time or two (or ten) that I was recently hospitalized again. This time it was for an abdominal incision hernia. Usually, this is outpatient surgery. However, the surgeon who made the original abdominal incision wanted to take no chances and arranged for me to stay in the hospital overnight. And that turned into five nights since he discovered another hernia under the one he’d expected to repair and then I kept running fevers. 

You probably know that you’re expected to start walking the day of (or the day after) surgery these days. It hastens your recovery. So, I walked the halls with the aid of a nurse and a walker, which fast became annoying although necessary (the walker, not the nurse). Apparently, I didn’t walk enough since for the time in her life, this 73 year developed bed sores.   

Photo by tegh 93 on Pexels.com

Bedsores? Certainly, that’s nothing to be ashamed of. Right? But there was that teeny little kernel of shame, as if I’d done something wrong and was being punished. Did it have to do with Chronic Kidney Disease? Why didn’t this happen during my other hospitalizations this last year? Of had I been just too out of it to realize I had bedsores during those hospitalizations?  

Come along with me as I figure this out. First of all, what are bedsores? The first thing I learned from my all-time favorite dictionary, The Merriam-Webster, at https://www.merriam-webster.com/dictionary/bedsores is that it’s one compound word, not two separate words as I’d always believed. Here’s their definition: 

“an ulceration of tissue deprived of adequate blood supply by prolonged pressure 

— called also decubitus ulcer” 

Wait a minute. What’s an ulcer? According to the same dictionary, but this time at https://www.merriam-webster.com/dictionary/ulcer

“a break in skin or mucous membrane with loss of surface tissue, disintegration and necrosis of epithelial tissue, and often pus” 

Okay, got it. Anyone know what “decubitus” means? I don’t. Back to the dictionary, guys. Well, will you look at that? The joke’s on us. That means “bedsore.” No kidding. Check it out for yourself at  https://www.merriam-webster.com/dictionary/decubitus.  

Now that we know what a bedsore is, let’s see if it has anything to do with CKD. Just keep in mind that diabetes is the foremost cause of CKD. This is from Beacon Health System at https://www.beaconhealthsystem.org/library/diseases-and-conditions/bedsores-pressure-ulcers/ , 

“Medical conditions affecting blood flow. Health problems that can affect blood flow, such as diabetes and vascular disease, can increase the risk of tissue damage such as bedsores.” 

Uh-oh, Type 2 diabetic here. 

Did you know there are stages of bedsores? I didn’t, but emedicine at  

https://emedicine.medscape.com/article/190115-overview educated me: 

” Stage 1 pressure injury – Nonblanchable erythema [Gail here: that means reddening.] of intact skin 

Stage 2 pressure injury – Partial-thickness skin loss with exposed dermis 

Stage 3 pressure injury – Full-thickness skin loss 

Stage 4 pressure injury – Full-thickness skin and tissue loss 

Unstageable pressure injury – Obscured full-thickness skin and tissue loss 

Deep pressure injury – Persistent nonblanchable deep red, maroon or purple discoloration” 

We know that dermis is skin, but “nonblanchable”? We can figure this out. If you remember your high school French, you know that ‘blanch’ means white. Add ‘non’ and we get ‘not white.’ That’s what nonblachable means; your skin does not turn white if you press on it.  

Wow! Lots of new information today. Okay, so how do you know if you have a bedsore? For me, it was the pain. I didn’t even have to look. 

The Mayo Clinic at https://www.mayoclinic.org/diseases-conditions/bed-sores/symptoms-causes/syc-20355893 tells us other symptoms: 

“Unusual changes in skin color or texture 

Swelling 

Pus-like draining 

An area of skin that feels cooler or warmer to the touch than other areas 

Tender areas” 

Come to think of it, the area in question was swollen, tender, and unusually warm. 

Now what? We know what bedsores are, what they have to do with CKD, that they are staged, and what the symptoms are. Ah, of course. What do you do once you have them? 

I was fortunate to come upon Johns Hopkins Medicine at https://www.hopkinsmedicine.org/health/conditions-and-diseases/bedsores for the answer to my question. 

  • “Removing pressure on the affected area 
  • Protecting the wound with medicated gauze or other special dressings 
  • Keeping the wound clean 
  • Ensuring good nutrition 
  • Removing the damaged, infected, or dead tissue (debridement) 
  • Transplanting healthy skin to the wound area (skin grafts) 
  • Negative pressure wound therapy 
  • Medicine (such as antibiotics to treat infections)” 

I’m thankful that removing the pressure on the affected area and a local antibiotic were all I needed. However, those were uncomfortable days for me and I’d like to avoid going through them again. 

Here’s what I should have been doing in the hospital according to Victoria State Government’s Better Health Channel (Canada),  

“Skin care in hospital 

During a stay in hospital, your skin may be affected by the hospital environment, staying in bed or sitting in one position for too long, whether you are eating and drinking enough and your physical condition. Ask hospital staff to regularly check your skin, particularly if you feel any pain. 

There are some things that you can do to look after your skin, including: 

Keep your skin clean and dry.  

Avoid any products that dry out your skin. This includes many soaps, body washes and talcum powder. Ask for skin cleansers that are non-drying. Ask nursing staff or your pharmacist to give you options. 

Use a water-based moisturiser daily. Be careful of bony areas and don’t rub or massage them. Ask staff for help if you need it. 

Check your skin every day or ask for help if you are concerned. Let a doctor or nurse know if there are any changes in your skin, especially redness, swelling or soreness. 

If you are at risk of pressure sores, a nurse will change your position often, including during the night. 

Always use any devices given to you to protect your skin from tearing and pressure sores. These may include protective mattresses, seat cushions, heel wedges and limb protectors.  

Drink plenty of water (unless the doctor has told you not to). 

Eat regular main meals and snacks. Sit out of bed to eat if you can. 

Try to maintain your regular toilet routine.  

If you have a wound, a plan will be developed with you and your family or carers before you leave hospital. It will tell you how to dress and care for the wound.”  

And here I’d been priding myself on sitting the chair from day one. I should have changing my position in that chair more often. 

Until next week, 

Keep living your life! 

Giving Credit Where Credit is Due

I’ve been feeling awfully thankful these past few weeks. Nothing like a health challenge or two to make you realize just how much you have to be grateful for. 

I’m not sure if you know it or not, but my husband – Paul Garwood, better known as Bear – has been my photographer for over a decade. Periodically I’ll think to mention it but, to be honest, haven’t mentioned that I am amazed by how he’s continued to do this (and do it well) despite his own health challenges. Thank you, Bear. 

But let’s not stop there. I’ve been highly active in the Chronic Kidney Disease Awareness Movement for over a decade. During that time, I’ve met others on the same path. The American Association of Kidney Patients has honored one of our own with a National Award and I’d like to honor him, too. 

“Organization Category: Urban Kidney Alliance, a Baltimore-based non-profit, focused on advocating, and empowering individuals in urban cities at-risk for chronic kidney disease (CKD) and other conditions. Award accepted by Founder, Steven Belcher, RN” 

Steve not only interviewed me on his show May 20th of this year, but guest blogged while I was laid up. Thank you, Steve. 

There are others, many in fact, that I’ve omitted. To you, I offer my apologies.   

My final gratitude for today’s blog goes to our kidneys. I’ve just learned that they produce glucose. Is that common knowledge? It was new to me and I wanted to know exactly how they do that. This is what sparked my interest: 

“…traditionally, the kidneys have not been considered an important source of glucose (except during acidosis or after prolonged fasting), with most clinical discussions on glucose dysregulation centering on the intestine, pancreas, liver, adipose tissue, and muscle…. More recently, however, the full significance of the kidneys’ contribution to glucose homeostasis, under both physiologic and pathologic conditions, has become well recognized, and is thought to involve functions well beyond glucose uptake and release. Besides the liver, the kidney is the only organ capable of generating sufficient glucose (gluconeogenesis) to release into the circulation, and it is also responsible for filtration and subsequent reabsorption or excretion of glucose…. These findings have provided considerable insight into the myriad of pathophysiologic mechanisms involved in the development of hyperglycemia and type 2 diabetes mellitus (T2DM) ….”  

The above is from AJMC at https://www.ajmc.com/view/ace005_12jan_triplitt_s11 and can probably use some explanation. First of all, AJMC is The American Journal of Managed Care and is actually for research outcomes. However, we find the information we need wherever we can. Let’s get to some of the explanations we may need. 

I started out by checking the glossary in What Is It and How Did I Get It? Early Stage Chronic Kidney Diseasethe first book I wrote about CKD way back in 2010. 

Glucose: The main sugar found in the blood. In diabetes, the body doesn’t adequately control natural and ingested sugar.” 

That helps, but we need more definitions. Thank goodness for my all-time favorite dictionary,The Merriam-Webster Dictionary: 

“acidosis: an abnormal condition characterized by reduced alkalinity of the blood and of the body tissues 

adipose tissue: connective tissue in which fat is stored and which has the cells distended by droplets of fat 

homeostasis: a relatively stable state of equilibrium or a tendency toward such a state between the different but interdependent elements or groups of elements of an organism, population, or group 

hyperglycemia: excess of sugar in the blood 

pathologic(al): … altered or caused by disease; also, indicative of disease 

pathophysiology: the physiology of abnormal states, specifically the functional changes that accompany a particular syndrome or disease 

physiologic(al): … characteristic of or appropriate to an organism’s healthy or normal functioning 

type 2 diabetes mellitus: a common form of diabetes mellitus that develops especially in adults and most often in obese individuals and that is characterized by hyperglycemia resulting from impaired insulin utilization coupled with the body’s inability to compensate with increased insulin production — called also non-insulin-dependent diabetes, non-insulin-dependent diabetes mellitus, type 2 diabetes mellitus” 

Can you hear me laughing? I’m beginning to feel like I’m back in the classroom teaching a vocabulary lesson. 

Okay, so what happens if we apply all these definitions to the AJMC quote? For one thing, the one that I found so surprising, we discover that the kidneys do generate glucose. Why is that so surprising, you ask. Well, if you’re like me, all you’ve known is that the kidneys regulate glucose. Hmmm, and how do they do that? 

According to Medscape.com at https://emedicine.medscape.com/article/983678-overview#a4

“Under normal circumstances, the kidney filters and reabsorbs 100% of glucose, approximately 180 g (1 mole) of glucose, each day. The glucose transporters expressed in the renal proximal tubule ensure that less than 0.5 g/day (range 0.03-0.3 g/d) is excreted in the urine of healthy adults. More water than glucose is reabsorbed resulting in an increase in the glucose concentration in the urine along the tubule. Consequently the affinity of the transporters for glucose along the tubule increases to allow for complete reabsorption of glucose from the urine.” 

I know, I know. We need to take a look at these tubules they talk about. That’s what Wikipedia is for. Take a look at https://bit.ly/3pqlF5k for more specific information. 

“The proximal tubule is the segment of the nephron in kidneys which begins from the renal pole of the Bowman’s capsule to the beginning of loop of Henle.” 

This goes back to basic kidney anatomy, but if you’re anything like me, you need a reminder every once in a while. Keep in mind, also, that ‘renal’ is another way of saying kidney. Rather than explain what the Bowman’s capsule and the loop of Henle are, I’ve included a good illustration above. So, the kidneys regulate the glucose in our blood just as they regulate waste products. 

Again and again, readers ask me questions to which I need to respond, “I’m not a doctor and have never claimed to be one. You really need to ask your nephrologist.” That’s the truth. When I write a blog about a topic – especially a reader requested topic – I’m learning, just as you are. 

Until next week, 

Keep living your life!  

Have You Heard of This?

Fabry’s Disease. I’ve noticed some posts on Facebook about this and now I’ve been invited to join the Kidneys and Fabry’s Disease group on Facebook. It’s amazing timing since I had decided the day before being asked to join the group that I’d be writing about it for today’s blog. The fun part for me is that I know absolutely nothing about this disease, so I get to explore it. 

The first thing I learned is that it has multiple names. The National Organization for Rare Disorders (NORD) at https://rarediseases.org/rare-diseases/fabry-disease/ lists them as: 

  • “alpha-galactosidase A deficiency 
  • Anderson-Fabry disease 
  • angiokeratoma corporis diffusum 
  • angiokeratoma diffuse 
  • GLA deficiency” 

We’ll use the name Fabry’s Disease for this blog. 

Let’s start at the beginning with an explanation of what it is. You’re going to have to read this slowly and carefully… or, at least, I did. It’s from The National Fabry Disease Organization at https://www.fabrydisease.org/index.php/about-fabry-disease/what-is-fabry-disease

“Fabry disease is a rare genetic disorder caused by a defective gene (the GLA gene) in the body. In most cases, the defect in the gene causes a deficient quantity of the enzyme alpha-galactosidase A. This enzyme is necessary for the daily breakdown (metabolism) of a lipid (fatty substance) in the body called globotriaosylceramide abbreviated GL-3 or GB-3. When proper metabolism of this lipid and other similar lipids does not occur, GL-3 accumulates in the majority of cells throughout the body. The resulting progressive lipid accumulation leads to cell damage. The cell damage causes a wide range of mild to severe symptoms including potentially life-threatening consequences such as kidney failure, heart attacks and strokes often at a relatively early age. Fabry disease is a progressive, destructive and potentially life-threatening disease. Fabry disease can affect males and females of all ethnic and cultural backgrounds.” 

That does not sound good. I wondered if there were symptoms. Remember that sometimes – like in my case – Chronic Kidney Disease doesn’t have symptoms. WebMd at https://www.webmd.com/a-to-z-guides/fabry-disease#1 tells us you may experience the following: 

“Pain and burning in your hands and feet that get worse with exercise, fever, hot weather, or when you’re tired 

Small, dark red spots usually found between your bellybutton and knees 

Cloudy vision 

Hearing loss 

Ringing in the ears 

Sweating less than normal 

Stomach pain, bowel movements right after eating” 

This is definitely something I wouldn’t want to play around with. Remember we discovered earlier in the blog that it’s genetic. That means you inherit it. Cedars-Sinai, a Los Angeles nonprofit academic healthcare organization at https://www.cedars-sinai.org/health-library/diseases-and-conditions/f/fabrys-disease.html informs us: 

“There is no cure for Fabry’s disease. However, in some cases the disease can be stopped from progressing if treated early enough. The first treatment generally is an enzyme replacement therapy which works to normalize the body’s ability to break down the fat.” 

Healthline (Yes, that Healthline) at https://www.healthline.com/health/fabry-disease explains that Fabry’s Disease can be very serious: 

“…. It’s progressive and can be life-threatening. People with FD have a damaged gene that leads to a shortage of an essential enzyme. The shortage results in a buildup of specific proteins in the body’s cells, causing damage to the: 

heart 

lungs 

kidneys 

skin 

brain 

stomach 

The disease affects both men and women in all ethnic groups, but men are usually more severely affected.” 

Hopefully, you noticed ‘kidneys’ in the list above. That is why I’ve included this disease in the kidney disease blogs. I want to remind you that this is a rare disease and that the purpose of the blog is to inform, not frighten. 

Further complicating our explanation is that there are two kinds of Fabry’s Disease. I turned to Fabry Disease News at https://fabrydiseasenews.com/type-2-fabry-disease/ for more information. 

“Fabry disease primarily has two recognized forms — type 1 (classical form) is the most severe and is associated with very little or no alpha-galactosidase activity, while type 2 (late-onset form) is milder with some residual enzyme activity.” 

This makes me think of Diabetes. Type 1 occurs when there is no insulin produced, while Type 2 occurs when there is insulin resistance and is a milder form of Diabetes. 

I wanted more about kidney disease and Fabry’s Disease so I kept poking around and I found it on The U.S. Department of Health and Human Services’ National Institutes of Health’s National Center for Advancing Translational Sciences’ Genetic and Rare Disease Information Center (That is one long title.) at https://bit.ly/325QD8K,  

ACE inhibitors may be used to treat decreased kidney function (renal insufficiency). ACE inhibitors can reduce the loss of protein in the urine (proteinuria). If kidney function continues to decrease dialysis and/or kidney transplantation may be necessary. A kidney transplanted successfully into a person with Fabry disease will remain free of the harmful build up of the fatty acid GL3 and therefore will restore normal kidney function. However it will not stop the buildup of GL3 in other organs or systems of the body. In addition, all potential donors that are relatives of the person with known Fabry disease should have their genetic status checked to make sure they do not have a pathogenic variant (mutation) in the GLA gene (even if they do not have symptoms).” 

Does this sound familiar? It’s also what can happen in CKD without involving the other organs, of course. 

The National Institute of Health’s National Institute of Neurological Disorders and Stroke at https://bit.ly/35RQ6Ze offers opportunities to join clinical trials and provides Fabry Disease patient organizations. The organizations listed presently are: 

Fabry Support & Information Group 

 
National Fabry Disease Foundation 

 
National Organization for Rare Disorders (NORD) 

 
National Tay-Sachs and Allied Diseases Association 

My head is spinning with all this new information right now and I suppose yours is, too. Maybe it’s time to stop and let us both digest it. 

Until next week, 

Keep living your life! 

Stress Is as Stress Does

I have been so stressed lately. It’s the usual: Covid-19, the elections, etc. But then there are the personal reasons: my upcoming surgery, Bear’s cataract surgery and being his caretaker, the third under-the-slab water leak in our house, and my brother’s ill health come to mind right away. I do take time to quietly read, play Word Crush, or watch a movie, but the stress is still there… and my blood glucose numbers are going up. “Is there a correlation?” I wondered. 

You may remember (I certainly do) that Healthline included this blog in the Best Kidney Disease Blogs for 2016 & 2017. They like my work; I like theirs, so I went to their website to see what I could find about stress and diabetes. I have diabetes type 2, by the way. That’s the type in which you produce insulin, but your body doesn’t use it well. 

Okay, now let’s see what Healthline at https://bit.ly/2TIHwWZ has to say: 

“… But there’s a problem. The body can’t differentiate between danger and stress. Both trigger fight-or-flight. 

So today’s most common ‘danger’ isn’t wild animals. It’s the letter from the IRS. There’s no quick resolution — no violent fight, no urgent need to run for miles. Instead, we sit in our sedentary homes and workplaces, our bodies surging with sugar, with no way to burn it off. 

That’s how stress messes with diabetes. Acute stress floods us with unwanted (and un-medicated) sugar. Chronic stress is like a leaking faucet, constantly dripping extra sugar into our systems. The impact on blood sugar caused by stress is so significant that some researchers feel it serves as a trigger for diabetes in people already predisposed to developing it.” 

Wait a minute here. “Acute stress floods us with unwanted (and un-medicated) sugar.” How does it do that? The answer I liked best is from Lark at https://bit.ly/3ebZU4b. Yes, Lark is a company that produces electronic aids for various stages of diabetes, but it also offers short, easy to understand explanations of what’s happening to your diabetes during different situations. 

“Cortisol signals your brain and body that it is time to prepare to take action. You may be able feel this as your heart pounds and muscles tense. At the same time, what you may not feel is that cortisol signals a hormone called glucagon to trigger the liver to release glucose (sugar) into your bloodstream. The result: higher blood sugar. 

Cortisol’s role in preparing your body for action goes beyond mobilizing glucose stores. Cortisol also works to make sure that the energy that you might spend (whether fighting a bear or running to stop your toddler from toddling into the street) gets replenished. That means you may feel hungry even when you do not truly need the food – and that can lead to weight gain. Again, the result is an increase in blood sugar.” 

Quick reminder: 

“Think of cortisol as nature’s built-in alarm system. It’s your body’s main stress hormone. It works with certain parts of your brain to control your mood, motivation, and fear. 

Your adrenal glands — triangle-shaped organs at the top of your kidneys — make cortisol. 

It’s best known for helping fuel your body’s ‘fight-or-flight’ instinct in a crisis, but cortisol plays an important role in a number of things your body does. For example, it: 

  • Manages how your body uses carbohydrates, fats, and proteins 
  • Keeps inflammation down 
  • Regulates your blood pressure 
  • Increases your blood sugar (glucose) 
  • Controls your sleep/wake cycle 
  • Boosts energy so you can handle stress and restores balance afterward” 

Thank you to WebMD at https://wb.md/35RaDgr for the above information. 

Let’s get back to how we end up with excess sugar in our blood due to both acute (sudden) and/or chronic (long term) stress. Diabetes Education Online, part of the Diabetes Teaching Center at the University of California, San Francisco, offers the following explanation. You can find out more by going to their website at https://bit.ly/3oNXgqi.    

“During stressful situations, epinephrine (adrenaline), glucagon, growth hormone and cortisol play a role in blood sugar levels. Stressful situations include infections, serious illness or significant emotion stress. 

When stressed, the body prepares itself by ensuring that enough sugar or energy is readily available. Insulin levels fall, glucagon and epinephrine (adrenaline) levels rise and more glucose is released from the liver. At the same time, growth hormone and cortisol levels rise, which causes body tissues (muscle and fat) to be less sensitive to insulin. As a result, more glucose is available in the blood stream.” 

Now I’m stressed about being stressed… and that’s after trying to keep my stress levels down so I don’t make my Chronic Kidney Disease worse… now I find it’s also making my diabetes worse. What, in heaven’s name, will happen if I continue to be this stressed? 

I went right to The National Kidney Foundation at https://bit.ly/2HQVsvs for an answer I could trust. 

“The combined impacts of increased blood pressure, faster heart rate, and higher fats and sugar in your blood can contribute to a number of health problems, including high blood pressure, diabetes, and heart disease (also known as cardiovascular disease). 

Stress and uncontrolled reactions to stress can also lead to kidney damage. As the blood filtering units of your body, your kidneys are prone to problems with blood circulation and blood vessels. High blood pressure and high blood sugar can place an additional strain or burden on your kidneys. People with high blood pressure and diabetes are at a higher risk for kidney disease. People with kidney disease are at higher risk for heart and blood vessel disease. If you already have heart and blood vessel disease and kidney disease, then the body’s reactions to stress can become more and more dangerous.” 

Oh, my! I think I’d better quietly read, play Word Crush, or watch a movie right now.  

Before I leave, I did want to let you know a $10 million Kidney Prize competition has been launched. If you’re seriously interested, go to https://akp.kidneyx.org. According to their website, KidneyX is 

“The Kidney Innovation Accelerator (KidneyX), a public-private partnership between the U.S. Department of Health and Human Services (HHS) and the American Society of Nephrology (ASN), is accelerating innovation in the prevention, diagnosis, and treatment of kidney diseases.” 

Until next week, 

Keep living your life! 

You Think It’s All in Your Head?

As I was sitting in my allergist’s office last week, I started to wonder if Chronic Kidney Disease had anything to do with my runny nose. I’d thought it was the usual seasonal allergies, but over the last dozen years or so I’ve learned that almost every malady I experience has some kind of relation to my kidneys…  so why not the runny nose? 

The American Kidney Fund at https://bit.ly/3kvpjb9 explains for us: 

“Granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis, is a disease that causes swelling and irritation of blood vessels in the kidneys, nose, sinuses, throat and lungs. Swollen blood vessels make it harder for blood to get to the organs and tissues that need it, which can be harmful. The disease also causes lumps called granulomas to form and damage the area around them. In some people GPA only affects the lungs. GPA that affects the kidneys can lead to chronic kidney disease and kidney failure.” 

Whoa! Not good. Let’s see how it’s treated. The Cleveland Clinic at https://cle.clinic/3mjudss tells us, 

“People with GPA who have critical organ system involvement are generally treated with corticosteroids [Gail here: commonly just called steroids] combined with another immunosuppressive medication such as cyclophosphamide (Cytoxan ®) or rituximab (Rituxan®). In patients who have less severe GPA, corticosteroids and methotrexate can be used initially. The goal of treatment is to stop all injury that is occurring as a result of GPA. If disease activity can be completely ‘turned off,’ this is called ‘remission.’ Once it is apparent that the disease is improving, doctors slowly reduce the corticosteroid dose and eventually hope to discontinue it completely. When cyclophosphamide is used, it is only given until the time of remission (usually around 3 to 6 months), after which time it is switched to another immunosuppressive agent, such as methotrexate, azathioprine (Imuran®), or mycophenolate mofetil (Cellcept®) to maintain remission. The treatment duration of the maintenance immunosuppressive medication may vary between individuals. In most instances, it is given for a minimum of 2 years before consideration is given to slowly reduce the dose toward discontinuation.” 

If this sounds familiar, you’re right. It’s straight out of this year’s May 25th blog. Aha! Now we see the value of using the category drop down to the right of the blog. 

Anyway, while this is interesting (to me, at least), it’s not answering my question: Can CKD cause sinus problems. What was that? You want to know what a runny nose has to do with your sinuses? Let’s find out.  

I returned to the ever-reliable Cleveland Clinic, this time at https://cle.clinic/2FXOm7Q,  for some information: 

“Sinusitis is an inflammation, or swelling, of the tissue lining the sinuses. The sinuses are four paired cavities (spaces) in the head. They are connected by narrow channels. The sinuses make thin mucus that drains out of the channels of the nose. This drainage helps keep the nose clean and free of bacteria. Normally filled with air, the sinuses can get blocked and filled with fluid. When that happens, bacteria can grow and cause an infection (bacterial sinusitis). 

This is also called rhinosinusitis, with ‘rhino’ meaning ‘nose.’ The nasal tissue is almost always swollen if sinus tissue is inflamed.” 

It seems that you need a runny nose to avoid sinusitis. Is that right? I don’t think so, and neither does MedicineNet at https://www.medicinenet.com/sinusitis/article.htm.  

“Sinusitis signs and symptoms include 

sinus headache, 

facial tenderness, 

pressure or pain in the sinuses, in the ears and teeth, 

fever, 

cloudy discolored nasal or postnasal drainage, [I bolded this symptom.] 

feeling of nasal stuffiness, 

sore throat, 

cough, and 

occasionally facial swelling.” 

So, now it seems that a runny nose can be a symptom of sinusitis. 

Photo by Andrea Piacquadio on Pexels.com

And how does that fit in with having CKD? Before we answer that, I think we need to straighten out the differences between allergy and cold symptoms since both conditions may cause sinusitis. 

“The symptoms of allergies and sinusitis overlap a lot. Both can give you a stuffy nose. If it’s allergies, you may also have: 

Runny nose and sneezing 

Watery or itchy eyes 

Wheezing 

If it’s sinusitis, besides a stuffy nose, you may have: 

Thick, colored mucus 

Painful, swollen feeling around your forehead, eyes, and cheeks 

Headache or pain in your teeth 

Post-nasal drip (mucus that moves from the back of your nose into your throat) 

Bad breath 

Cough and sore throat 

Fatigue 

Light fever” 

Thank you to WebMD at https://www.webmd.com/allergies/sinusitis-or-allergies for the list above.  

 On to my original question. This is from Vick’s at https://vicks.com/en-us/treatments/how-to-treat-a-cold/how-to-stop-a-runny-nose. (Who better to go to than a trusted friend since childhood?)  

“A runny nose is a discharge of mucus from the nostrils. It’s the result of excess nasal mucus production. The excess nasal mucus leads to watery nasal secretions that flow out of your nostrils or drip down into your throat. A runny nose is a discharge of mucus from the nostrils. It’s the result of excess nasal mucus production. The excess nasal mucus leads to watery nasal secretions that flow out of your nostrils or drip down into your throat. Nasal congestion is due to the inflammation of the linings of the nasal cavity.” 

Did you notice the word “inflammation” in the last sentence? Ahem, an article by Oleh M Akchurin of Weill Cornell Medical College and Frederick J Kaskel of Albert Einstein College of Medicine published by ResearchGate at https://bit.ly/3jtVzKL states: 

“Chronic inflammation should be regarded as a common comorbid condition in CKD and especially in dialysis patients.”   

And there you have it. Your (and my) runny nose can be caused – in part – from having CKD. Inflammation is the name of the game if you have Chronic Kidney Disease. 

Although, in these times, I wonder if Covid-19 might somehow be involved in certain cases. Just remember, I’m not a doctor and never claimed to be one, so this just might be a question for your medical provider. 

Until next week, 

Keep living your life! (Safely: mask up, wash up, social distance) 
 

Cellulitis, CKD, and Diabetes

My uncle-in-law had it. My children’s father had it. My husband had it. Now the question is what is cellulitis? 

WebMd at https://www.webmd.com/skin-problems-and-treatments/guide/cellulitis#1 answers: 

“Cellulitis is a common infection of the skin and the soft tissues underneath. It happens when bacteria enter a break in the skin and spread. The result is infection, which may cause swelling, redness, pain, or warmth.” 

Alright, but what does that have to do with Chronic Kidney Disease. By the way, only one of the men mentioned in the first paragraph has CKD.  

According to the NHS (National Health Service) in the United Kingdom at https://bit.ly/2IJJrbT:&nbsp;

“You’re more at risk of cellulitis if you: 

  • have poor circulation in your arms, legs, hands or feet – for example, because you’re overweight 
  • find it difficult to move around 
  • have a weakened immune system because of chemotherapy treatment or diabetes [Gail here: I bolded that.] 
  • have bedsores (pressure ulcers) 
  • have lymphoedema, which causes fluid build-up under the skin 
  • inject drugs 
  • have a wound from surgery 
  • have had cellulitis before” 

Two of the men above were overweight, but one of these did not have CKD. The overweight man who had CKD also had diabetes. One had a wound from surgery which was the cause of his cellulitis. Another had had cellulitis before. (Does this sound like one of those crazy math word questions?) 

CKD is not a cause? Whoa! Whoa! Whoa! Wait just a minute here. Let’s remember that CKD gives you the lovely present of a compromised immune system. A compromised immune system means it doesn’t do such a great job of preventing illnesses and infections. 

Also remember that diabetes is the leading cause of CKD and diabetes can also weaken your immune system. I needed more information about diabetes doing that and I got it from The University of Michigan’s Michigan Medicine at https://www.uofmhealth.org/health-library/uq1148abc:    

“High blood sugar from diabetes can affect the body’s immune system, impairing the ability of white blood cells to come to the site of an infection, stay in the infected area, and kill microorganisms. Because of the buildup of plaque in blood vessels associated with diabetes, areas of infection may receive a poor blood supply, further lowering the body’s ability to fight infections and heal wounds.” 

Remember that cellulitis is an infection. Reading the above, I became aware that I didn’t know anything about plague in the blood vessels and diabetes, so I went right to what I consider the source for vascular information, Vascular.org. This time at https://bit.ly/31dZ0yI:  

“Peripheral artery (or arterial) disease, also known as PAD, occurs when plaque builds up in the arteries and reduces blood flow to the feet and legs. Fairly common among elderly Americans, PAD is even more likely among those with diabetes, which increases plaque buildup.” 

All three of these men were elderly, if you consider in your 70s elderly. Of course, I don’t since I’m in my 70s, but we are talking science here. 

Hmmm, we don’t know yet how cellulitis is treated, do we? Let’s find out. I turned to my old buddy, The MayoClinic at https://www.mayoclinic.org/diseases-conditions/cellulitis/diagnosis-treatment/drc-20370766:  

“Cellulitis treatment usually includes a prescription oral antibiotic. Within three days of starting an antibiotic, let your doctor know whether the infection is responding to treatment. You’ll need to take the antibiotic for as long as your doctor directs, usually five to 10 days but possibly as long as 14 days. 

In most cases, signs and symptoms of cellulitis disappear after a few days. You may need to be hospitalized and receive antibiotics through your veins (intravenously) if: 

Signs and symptoms don’t respond to oral antibiotics 

Signs and symptoms are extensive 

You have a high fever 

Usually, doctors prescribe a drug that’s effective against both streptococci and staphylococci. It’s important that you take the medication as directed and finish the entire course of medication, even after you feel better. 

Your doctor also might recommend elevating the affected area, which may speed recovery…. 

Try these steps to help ease any pain and swelling: 

Place a cool, damp cloth on the affected area as often as needed for your comfort. 

Ask your doctor to suggest an over-the-counter pain medication to treat pain. [Gail again: no NSAIDS, you have CKD.] 

Elevate the affected part of your body.” 

Now the obvious question is how, as CKD patients and possibly diabetics, do we avoid that infection in the first place? 

“Cellulitis cannot always be prevented, but the risk of developing cellulitis can be minimised by avoiding injury to the skin, maintain [sic] good hygiene and by managing skin conditions like tinea and eczema. 

A common cause of infection to the skin is via the fingernails. Handwashing is very important as well as keeping good care of your nails by trimming and cleaning them. Generally maintaining good hygiene such as daily showering and wearing clean clothes may help reduce the skin’s contact with bacteria. 

If you have broken skin, keep the wound clean by washing daily with soap and water or antiseptic. Cover the wound with a gauze dressing or bandaid every day and watch for signs of infection. 

People who are susceptible to cellulitis, for example people with diabetes or with poor circulation, should take care to protect themselves with appropriate footwear, gloves and long pants when gardening or bushwalking, when it’s easy to get scratched or bitten. Look after your skin by regularly checking your feet for signs of injury, moisturising the skin and trimming fingernails and toenails regularly.” 

Thank you to Australia’s HealthDirect at https://www.healthdirect.gov.au/cellulitis-prevention for these common sense reminders. Actually, we need to keep washing our hands while Covid-19 is at our door anyway, so we’ve already got that part of the prevention covered. I suspect that many of us don’t bother to deal with small wounds, but it looks like we’d better start. 

What if you do develop cellulitis? How will you be treated? My old buddy, The Mayo Clinic at https://mayocl.in/2FDxUtf tells us: 

“Cellulitis treatment usually includes a prescription oral antibiotic. Within three days of starting an antibiotic, let your doctor know whether the infection is responding to treatment. You’ll need to take the antibiotic for as long as your doctor directs, usually five to 10 days but possibly as long as 14 days. 

In most cases, signs and symptoms of cellulitis disappear after a few days. You may need to be hospitalized and receive antibiotics through your veins (intravenously) if: 

Signs and symptoms don’t respond to oral antibiotics 

Signs and symptoms are extensive 

You have a high fever 

Usually, doctors prescribe a drug that’s effective against both streptococci and staphylococci. It’s important that you take the medication as directed and finish the entire course of medication, even after you feel better. 

Your doctor also might recommend elevating the affected area, which may speed recovery.” 

Until next week, 

Keep living your life! (Safely, please) 

 

Oh, S**T!

Cute, huh? Especially since I’ll be writing about feces or, as it’s commonly called these days, poo. Defecation (or pooing, if you’d rather) is an important topic for those of us with Chronic Kidney Disease. Did you know CKD can lead to constipation? 

Photo by Pixabay on Pexels.com

Well, how do you know if you have constipation? The Mayo Clinic at https://www.mayoclinic.org/diseases-conditions/constipation/symptoms-causes/syc-20354253 explains: 

  • “Passing fewer than three stools a week 
  • Having lumpy or hard stools 
  • Straining to have bowel movements 
  • Feeling as though there’s a blockage in your rectum that prevents bowel movements 
  • Feeling as though you can’t completely empty the stool from your rectum 
  • Needing help to empty your rectum, such as using your hands to press on your abdomen and using a finger to remove stool from your rectum” 

Sometimes, medication can be the cause of constipation. According to the International Foundation of Gastrointestinal Disorders at https://www.iffgd.org/diet-treatments/medications/medications-that-can-affect-colonic-function.html

“Constipation can be caused by a variety of medications. These medications affect the nerve and muscle activity in the large intestine (colon) and may also bind intestinal liquid. This may result in slowed colonic action (slow and/or difficult passing of stool).” 

Maybe we need to know what happens in your body during constipation? This is what the Cleveland Clinic at https://my.clevelandclinic.org/health/diseases/4059-constipation has to say: 

“Constipation happens because your colon absorbs too much water from waste (stool/poop), which dries out the stool making it hard in consistency and difficult to push out of the body. 

To back up a bit, as food normally moves through the digestive tract, nutrients are absorbed. The partially digested food (waste) that remains moves from the small intestine to the large intestine, also called the colon. The colon absorbs water from this waste, which creates a solid matter called stool. If you have constipation, food may move too slowly through the digestive tract. This gives the colon more time – too much time – to absorb water from the waste. The stool becomes dry, hard, and difficult to push out.” 

Photo by August de Richelieu on Pexels.com

We’re Chronic Kidney Disease patients. That means some of the foods recommended to alleviate constipation may not be allowed on our renal diets. For instance, dried raisin, apricots, and prunes are too high in potassium for CKD patients, although they are helpful if you’re experiencing constipation. You need to speak with your renal dietitian before changing your diet. 

I turned to a new site, BMC at https://rrtjournal.biomedcentral.com/articles/10.1186/s41100-019-0246-3 for information about constipation that is particular to CKD patients. BMC has “an evolving portfolio of some 300 peer-reviewed journals, sharing discoveries from research communities in science, technology, engineering and medicine,” as stated on their website.   

“Accumulating evidence has revealed a relationship between constipation and cardiovascular disease and CKD. The pathogenesis of constipation in CKD patients is multifactorial: decreased physical activity, comorbidities affecting bowel movement, such as diabetes mellitus, cerebrovascular disease, and hyperparathyroidism, a restricted dietary intake of plant-based fiber-rich foods, and multiple medications, including phosphate binders and potassium-binding resins, have all been implicated. CKD is associated with alterations in the composition and function of the gut microbiota, so-called gut dysbiosis.” 

Oh goody, a term I don’t know. Remember VeryWell Health? This is their definition of gut dysbiosis at https://www.verywellhealth.com/what-is-intestinal-dysbiosis-1945045#:~:text=Overview,the%20microorganisms%20within%20our%20intestines

“Gut microbiota dysbiosis, also known as intestinal or gastrointestinal dysbiosis, refers to a condition in which there is an imbalance of the microorganisms within our intestines. These microorganisms, collectively known as gut flora, consist predominantly of various strains of bacteria, and to a lesser extent include fungi and protozoa. The gut flora are essential for digestion and immune functioning….  A state of dysbiosis, therefore, will result in digestive and other systemic symptoms.” 

Photo by Anna Shvets on Pexels.com

Aha, so that’s why I take probiotics. I not only have CKD, but Diabetes Type 2, and have had chemotherapy which is known to cause this problem. I always wondered what the probiotics did for me. We’ll find out right now. WebMD at https://www.webmd.com/digestive-disorders/what-are-probiotics was helpful here: 

“Researchers are trying to figure out exactly how probiotics work. Some of the ways they may keep you healthy: 

  • When you lose ‘good’ bacteria in your body, for example after you take antibiotics, probiotics can help replace them. 
  • They can help balance your ‘good’ and ‘bad’ bacteria to keep your body working the way it should.” 

Prebiotics are also recommended. I get it that ‘pre’ is a suffix (group of letters added before a word to change its meaning) indicating ‘before,’ but still, what do they do for us?  Here’s what the Mayo Clinic at https://www.mayoclinic.org/prebiotics-probiotics-and-your-health/art-20390058 has to say about prebiotics, 

“Prebiotics are specialized plant fibers. They act like fertilizers that stimulate the growth of healthy bacteria in the gut. 

Prebiotics are found in many fruits and vegetables, especially those that contain complex carbohydrates, such as fiber and resistant starch. These carbs aren’t digestible by your body, so they pass through the digestive system to become food for the bacteria and other microbes.” 

To sum it all up: 

“Constipation is one of the most common gastrointestinal disorders among patients with chronic kidney disease (CKD) partly because of their sedentary lifestyle, low fiber and fluid intake, concomitant medications (e.g., phosphate binders), and multiple comorbidities (e.g., diabetes). Although constipation is usually perceived as a benign, often self-limited condition, recent evidence has challenged this most common perception of constipation. The chronic symptoms of constipation negatively affect patients’ quality of life and impose a considerable social and economic burden. Furthermore, recent epidemiological studies have revealed that constipation is independently associated with adverse clinical outcomes, such as end-stage renal disease (ESRD), cardiovascular (CV) disease, and mortality, potentially mediated by the alteration of gut microbiota and the increased production of fecal metabolites. Given the importance of the gut in the disposal of uremic toxins and in acid-base and mineral homeostasis with declining kidney function, the presence of constipation in CKD may limit or even preclude these ancillary gastrointestinal roles, potentially contributing to excess morbidity and mortality….” 

Thank you to the National Institutes of Health’s U.S. Library of Medicine’s National Center for Biotechnology Information at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7000799/ for their summary of the problem. Before I end this blog, I ask you to make sure you notice the mention of “the disposal of uremic toxins” above. 

Until next week, 

Keep living your life!