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! 

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! 

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: 

“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! 

Baby, It’s Hot Outside.

As a person with arthritis among other maladies, I regularly see my rheumatologist. “A rheumatologist is a board certified internist or pediatrician who is qualified by additional training and experience in the diagnosis and treatment of arthritis and other diseases of the joints, muscles, and bones,” according to HSS at https://www.hss.edu/rheumatology-rheumatologist.asp. During my appointment, she mentioned that my GFR (Glomerular Filtration Rate) was 46.

Panic! It’s almost always in the low 50s. She calmed me down by telling me that GFR is usually lower during the Arizona heat (I know, I know: but it’s a dry heat.) of the summer. I don’t know why I was surprised. It made sense.

Think about it. Let me re-enforce this with a statement taken from study on PubMed at https://pubmed.ncbi.nlm.nih.gov/21617334/.

“However, the percent change in eGFR from spring to summer was greater in hypertensive patients with CKD… than in those without CKD …. “

PubMed is part of the National Institutes of Health’s National Library of Medicine’s National Center for Biotechnology Information.

I know hypertension (high blood pressure) is included in this statement, but the fact that GFR is lowered t than it’s lowered in those without hypertension leads us to the realization that those without hypertension DO have lower GFRs during the summer heat.

Another study from EuropePMC at https://europepmc.org/article/med/28946962 tells us:

“Recurrent dehydration in people regularly exposed to high temperatures seems to be resulting in an unrecognised cause of proteinuric chronic kidney disease, the underlying pathophysiological mechanism of which is becoming better understood. However, beyond heat waves and extreme temperatures, there is a seasonal variation in glomerular filtration rate that may contribute to the onset of renal failure and electrolyte disorders during extremely hot periods.”

Here are a couple of definitions you may need to understand the above statement. The first is from The Mayo Clinic at https://www.mayoclinic.org/symptoms/protein-in-urine/basics/definition/sym-20050656.

“Protein in urine — known as proteinuria (pro-tee-NU-ree-uh) — is excess protein found in a urine sample. Protein is one of the substances identified during a test to analyze the content of your urine (urinalysis).

Low levels of protein in urine are normal. Temporarily high levels of protein in urine aren’t unusual either, particularly in younger people after exercise or during an illness.

Persistently high levels of protein in urine may be a sign of kidney disease.”

The following definition is from MedicineNet at https://www.medicinenet.com/script/main/art.asp?articlekey=10691.

“Pathophysiology: Deranged function in an individual or an organ due to a disease.”

So, it looks like dehydration is a key factor in lowering the GFR during the summer heat. We know that dialysis patients need to limit their liquid intake, but what about those of us who are not on dialysis but do have CKD (Chronic Kidney Disease)?

I went to MedicalNewsToday at https://www.medicalnewstoday.com/articles/153363#symptoms for some facts about dehydration:

“Around three-quarters of the human body is water.

The causes of dehydration include diarrhea, vomiting, and sweating.

Individuals more at risk of dehydration include athletes, people at higher altitudes, and older adults.

Early symptoms of dehydration include dry mouth, lethargy, and dizziness.”

Did you notice “sweating” and for those of a certain age like me “older adults”?

So, I gather I’m sweating out more liquids than I’m taking in. But how does that work exactly? I thought I was drinking sufficient amounts of fluid.

Biology Online at https://www.biologyonline.com/dictionary/sweating was a bit of an eye opener.

“Sweating is a way of our body to regulate body temperature. It is commonly used as a synonym for perspiration but in stricter sense perspiration pertains to the water loss as a cooling mechanism of the body and therefore It (sic) includes both the release of watery, salty fluid through the pores of the skin from the sweat glands and the evaporation of water from the skin (trans-epithelial) and respiratory tract. Thus, there exist two forms of perspiration, the sensible and the insensible water loss. In sweating, the process always entails the loss of both water and solutes…. The salty fluid is secreted as droplets or moist on the skin and is called as sweat. Environmental cues that could stimulate the body to produce sweat are high temperature and humidity of the surroundings.”

Oh, solutes. Those include the electrolytes that are so important to us as CKD patients. Orthology at https://orthology.com/myth-debunked-need-electrolytes-work/ offers us a simple explanation:

“The warmer the weather and the more you sweat, the more likely you’ll need electrolyte replacement. Again, this is just a general guideline and will differ by individual, activity and other factors. Pay attention to signs that your electrolyte levels are too low, such as muscle cramps, fatigue, dizziness, nausea or mental confusion.”

Aha, it’s excessively hot out. We drink more, but more sweat is being produced the higher the temperature is. When we sweat or perspire (since the two words are often used interchangeably), we are also exuding electrolytes. Now it all makes sense. An imbalance of electrolytes could lower your GFR. I turned to Tampa Cardio at https://tampacardio.com/causes-electrolyte-imbalance-body/ for confirmation.

“Electrolyte imbalances can cause a wide range of symptoms, some mild and some potentially life threatening. Electrolyte imbalances are commonly caused by loss of fluids through prolonged diarrhea, vomiting, sweating or high fever.”

But we’re already having problems with our electrolytes. No wonder excessive heat affects our GFR. As the University of Michigan’s Michigan Medical at https://www.uofmhealth.org/conditions-treatments/kidney/fluid-and-electrolyte-disorders states:

“Changes in the body’s levels of minerals including potassium, magnesium, calcium and sodium—and the corresponding impact these have on the body’s function, muscle strength and heart rhythm can be associated with disorders of kidney or endocrine glands.

Got it. Let’s all just stay in the air conditioning so we don’t lower our GFRs even more than the excessive heat does. In Arizonia, that probably means until November this year. That was a joke (I hope).

Until next week,

Keep living your life!

They Go Together… Sometimes 

I’m certain you’ve already read about Covid-19 causing Acute Kidney Injury (AKI). To the best of our knowledge, it’s airborne which means the lungs are involved. But did you know there’s a correlation between the lungs and the kidneys?

Think of it this way. You know Chronic Kidney Disease (CKD) can be the cause of diabetes (sigh, that’s me) or hypertension (high blood pressure). You also know that hypertension can be the cause of CKD (sigh, that’s me again.) Well, AKI can be the cause of Acute Lung Disease (ALI) and ALI can be the cause of Acute Kidney Disease.

I know I just blindsided you with a new medical term, so let’s find out just what ALI is.  I went to The National Organization for Rare Disorders at https://rarediseases.org/rare-diseases/acute-respiratory-distress-syndrome/ for what turned out to be a rather comprehensive answer:

“Acute respiratory distress syndrome (ARDS) is a type of severe, acute lung dysfunction affecting all or most of both lungs that occurs as a result of illness or injury. Although it is sometimes called adult respiratory distress syndrome, it may also affect children. ARDS is a buildup of fluid in the small air sacs (alveoli) in the lungs. This makes it difficult for oxygen to get into the bloodstream.”

Ah, so ALI and Acute Respiratory Distress Syndrome (ARDS) are one and the same. That should make finding information about it a bit easier.

We’ve just learned that ALI can cause AKI and vice-versa, but what can cause ALI beside Covid-19? This list is from the Mayo Clinic at https://www.mayoclinic.org/diseases-conditions/ards/symptoms-causes/syc-20355576. Notice they do include COVID-19 as a cause of ARDS.

  • “Sepsis. The most common cause of ARDS is sepsis, a serious and widespread infection of the bloodstream.
  • Inhalation of harmful substances. Breathing high concentrations of smoke or chemical fumes can result in ARDS, as can inhaling (aspirating) vomit or near-drowning episodes.
  • Severe pneumonia. Severe cases of pneumonia usually affect all five lobes of the lungs.
  • Head, chest or other major injury. Accidents, such as falls or car crashes, can directly damage the lungs or the portion of the brain that controls breathing.
  • Coronavirus disease 2019 (COVID-19). People who have severe COVID-19 may develop ARDS.
  • Others. Pancreatitis (inflammation of the pancreas), massive blood transfusions and burns.”

We can probably guess that one of the symptoms of ALI or ARDS is breathlessness, but let’s see if there are any others. I decided to go to Healthline at https://www.healthline.com/health/acute-respiratory-distress-syndrome#symptoms for this information. Yep, breathlessness is not the only symptom of ARDS.

  • “labored and rapid breathing
  • muscle fatigue and general weakness
  • low blood pressure
  • discolored skin or nails
  • a dry, hacking cough
  • a fever
  • headaches
  • a fast pulse rate
  • mental confusion”

This is not looking good at all. I’m wondering how ALI is treated now. The American Lung Association at https://www.lung.org/lung-health-diseases/lung-disease-lookup/ards/ards-treatment-and-recovery was detailed in explaining.

Ventilator support

All patients with ARDS will require extra oxygen. Oxygen alone is usually not enough, and high levels of oxygen can also injure the lung. A ventilator is a machine used to open airspaces that have shut down and help with the work of breathing. The ventilator is connected to the patient through a mask on the face or a tube inserted into the windpipe.

Prone positioning

ARDS patients are typically in bed on their back. When oxygen and ventilator therapies are at high levels and blood oxygen is still low, ARDS patients are sometimes turned over on their stomach to get more oxygen into the blood. This is called proning and may help improve oxygen levels in the blood for a while. It is a complicated task and some patients are too sick for this treatment.

Sedation and medications to prevent movement

To relieve shortness of breath and prevent agitation, the ARDS patient usually needs sedation. Sometimes added medications called paralytics are needed up front to help the patient adjust to the ventilator. These medications have significant side effects and their risks and benefits must be continuously monitored.

Fluid management

Doctors may give ARDS patients a medication called a diuretic to increase urination in hopes of removing excess fluid from the body to help prevent fluid from building up in the lungs. This must be done carefully, because too much fluid removal can lower blood pressure and lead to kidney problems.

Extracorporeal membrane oxygenation (ECMO)

ECMO is a very complicated treatment that takes blood outside of your body and pumps it through a membrane that adds oxygen, removes carbon dioxide and then returns the blood to your body. This is a high-risk therapy with many potential complications. It is not suitable for every ARDS patient.”

Now that we understand what ALI/ARDS is, what – in heaven’s name – does it have to do with AKI?

“Renal failure is a frequent complication of ARDS, particularly in the context of sepsis. Renal failure may be related to hypotension, nephrotoxic drugs, or underlying illness. Fluid management is complicated in this context, especially if the patient is oliguric. Multisystem organ failure, rather than respiratory failure alone, is usually the cause of death in ARDS.”

Thank you Medscape at https://www.medscape.com/answers/165139-43289/why-is-renal-failure-a-frequent-complication-of-acute-respiratory-distress-syndrome-ards for the explanation.  I think a few definitions are in order to adequately understand this explanation.

“Sepsis refers to a bacterial infection in the bloodstream or body tissues. This is a very broad term covering the presence of many types of microscopic disease-causing organisms.

Hypotension is the medical term for low blood pressure.

Nephrotoxic is toxic, or damaging, to the kidney.

(Oligoric is the adjective meaning of or pertaining to oligoria.)

Oliguria or oliguresis is the noun meaning the excretion of an abnormally small volume of urine, often as the result of a kidney disorder.”

All the above definitions were paraphrased from The Free Dictionary by Farlex, Medical Dictionary.

You probably know more than you wanted to about the connection between Covid-19, your lungs, and your kidneys than you ever intended to find out by now. Don’t be frightened, but do wear your mask and continue to social distance. Oh, and don’t forget the hand sanitizer.

Until next week,

Keep living your life!

“klot” + “id” 

No, that’s not the result of misplacing my fingers on the keyboard. According to https://youglish.com/pronounce/clotted/english, this is the correct two syllable pronunciation of the word clotted. My all-time favorite dictionary, the Merriam-Webster, at https://www.merriam-webster.com/dictionary/clotted defines the adjective (word describing a noun) clotted as:

“1: a portion of a substance adhering together in a thick nondescript mass (as of clay or gum)

2 a: a roundish viscous lump formed by coagulation of a portion of liquid or by melting

b: a coagulated mass produced by clotting of blood”

You’re right – it’s the second definition we’ll be dealing with today. Why? A long-time reader was telling me about his blood clot when I suddenly realized I had no idea if there were any connection at all between Chronic Kidney Disease and blood clots.

As it turns out, there is.  The following is from the National Kidney Foundation at https://www.kidney.org/sites/default/files/Blood_Clots_And_CKD_2018.pdf:

“CKD may put you at higher risk for VTE. The reasons for this are not well understood. The connection may depend on what caused your CKD and how much kidney damage you have. No matter the reason, CKD may make it easier for your body to form blood clots. The risk for VTE is seen more often in people with nephrotic syndrome (a kidney problem that causes swelling, usually of the ankles, a high level of protein in the urine, and a low level of a protein called albumin in the blood).”

I have a question already. What is VTE? I found World Thrombosis Day’s explanation at www.worldthrombosisday.org › issue › vte the most helpful.

“Venous thromboembolism (VTE) is a condition in which a blood clot forms most often in the deep veins of the leg, groin or arm (known as deep vein thrombosis, DVT) and travels in the circulation, lodging in the lungs (known as pulmonary embolism, PE).”

How could I have CKD for over a dozen years and not know this? Many thanks to my reader and online friend for bringing it up. 

Well, it’s back to the beginning for us. How is VTE diagnosed? The Centers for Disease Control and Prevention (CDC) at www.cdc.gov › ncbddd › dvt › diagnosis-treatment was helpful here.

“Duplex ultrasonography is an imaging test that uses sound waves to look at the flow of blood in the veins. It can detect blockages or blood clots in the deep veins. It is the standard imaging test to diagnose DVT. A D-dimer blood test measures a substance in the blood that is released when a clot breaks up.”

Let’s take a closer look at the D-dimer blood test. That’s another new one for me. My old standby, MedlinePlus (This time at https://medlineplus.gov/lab-tests/d-dimer-test/.) offered the following which more than satisfactorily answered my question.

“A D-dimer test looks for D-dimer in blood. D-dimer is a protein fragment (small piece) that’s made when a blood clot dissolves in your body.

Blood clotting is an important process that prevents you from losing too much blood when you are injured. Normally, your body will dissolve the clot once your injury has healed. With a blood clotting disorder, clots can form when you don’t have an obvious injury or don’t dissolve when they should. These conditions can be very serious and even life-threatening. A D-dimer test can show if you have one of these conditions.”

By the way, MedlinePlus is part of the U.S. National Library of Medicine which, in turn, is part of the National Institutes of Health.

This brings me to another question. How would you or your doctor even know you may need this test?

“According to the Centers for Disease Control and Prevention (CDC), about half of people with DVT don’t have symptoms. Any symptoms that do occur will be in the affected leg or the area where the clot is found. Symptoms can include:

pain

redness of the skin

warmth of the skin

swelling of the area

If the clot moves into the lungs and you develop PE, you may have symptoms such as:

chest pain, which may get worse when you breathe deeply or cough

coughing

coughing up blood

dizziness or even fainting

rapid shallow breathing, or tachypnea

rapid heartbeat

irregular heartbeat

shortness of breath”

Thank you to Healthline at https://www.healthline.com/health/dvt-vs-pulmonary-embolism for the above information.

Now we know what VTE is, what symptoms you may experience, and the test to take to confirm that you do, indeed, have VTE. You know what comes next. How do we treat VTE once it’s confirmed?

These are some, but not all, of the treatments that may be recommended. I discovered them on WebMD’s site at https://www.webmd.com/dvt/what-is-venous-thromboembolism.

“Blood thinners. These drugs don’t break up the clot, but they can stop it from getting bigger so your body has time to break it down on its own. They include heparin, low-molecular-weight heparin, apixaban (Eliquis), edoxaban (Savaysa), rivaroxaban (Xarelto), and warfarin (Coumadin).

Clot-busting drugs. These medicines are injections that can break up your clot. They include drugs like tPA (tissue plasminogen activator).

Surgery. In some cases, your doctor may need to put a special filter into a vein, which can stop any future clots from getting to your lungs. Sometimes, people need surgery to remove a clot.

Even after you recover from a VTE and you’re out of the hospital, you’ll probably still need treatment with blood thinners for at least 3 months. That’s because your chances of having another VTE will be higher for a while.”

I’m still wondering how to avoid VTE. This is what The National Blood Clot Alliance at https://www.stoptheclot.org/learn_more/prevention_of_thrombosis/ suggested:

“Ask your doctor about need for ‘blood thinners’ or compression stockings to prevent clots, whenever you go to the hospital

Lose weight, if you are overweight

Stay active

Exercise regularly; walking is fine

Avoid long periods of staying still

Get up and move around at least every hour whenever you travel on a plane, train, or bus, particularly if the trip is longer than 4 hours

Do heel toe exercises or circle your feet if you cannot move around

Stop at least every two hours when you drive, and get out and move around

Drink a lot of water and wear loose fitted clothing when you travel

Talk to your doctor about your risk of clotting whenever you take hormones, whether for birth control or replacement therapy, or during and right after any pregnancy

Follow any self-care measures to keep heart failure, diabetes, or any other health issues as stable as possible”

And we have yet another reason to be extra cautious if you have CKD.

Until next week,

Keep living your life!

 

Keep It Where It Belongs 

You’ve all read about my cancer dance in one blog or another. Thank goodness, that’s over. But there are residual effects like hand and foot neuropathy, chemo brain (akin to CKD’s brain fog), and – to my great surprise – abdominal incisional hernia after surgery. How did that happen, I wondered.

Get ready for this: those with Chronic Kidney Disease have a 12.8% higher incidence of abdominal incisional hernia according to a PubMed 2013 study published on ResearchGate’s site available at https://bit.ly/3kdvxfl,

“Chronic kidney disease is associated with impaired wound healing and constitutes an independent risk factor for incisional hernia development.”

(The percentage of abdominal incisional hernia among CKD patients was taken from the cohort in this abstract.)

According to the same study:

“Elevated uremia toxins may inhibit granulation tissue formation and impair wound healing, thereby promoting incisional hernia development.”

As Chronic Kidney Disease patients, we know the accumulation of uremia toxins as uremia. On to my favorite dictionary, the Merriam-Webster at https://www.merriam-webster.com/dictionary/uremia for a definition of uremia:

“1: accumulation in the blood of constituents normally eliminated in the urine that produces a severe toxic condition and usually occurs in severe kidney disease

2: the toxic bodily condition associated with uremia”

It gets worse. First, you have to know that I am considered ‘elderly,’ another surprise.  According to The World Health Organization at https://bit.ly/32sQq05:

“Most developed world countries have accepted the chronological age of 65 years as a definition of ‘elderly’ or older person….”

I’m 73 and here’s why you needed this information that I am of advancing age.

“The risk factors for incisional hernia following abdominal surgery include (ranked by relative risk):

Emergency surgery

Emergency surgery carries double the risk of elective surgery.

Wound type

BMI >25

Obese patients are more likely to develop an incisional hernia

Midline incision

There is a 74% risk increase compared to non-midline

Wound infection

This increases incisional hernia risk by 68%.

Pre-operative chemotherapy

Intra-operative blood transfusion

Advancing age

Pregnancy

Other less common risk factors include chronic cough, diabetes mellitus, steroid therapy, smoking, and connective tissue disease.”

Thank you TeachMeSurgery at https://bit.ly/2GYrOUH for this risk factor information.

I have so many risks factors. Foremost for me, of course, is Chronic Kidney Disease as demonstrated earlier in this blog, but also advancing age. Oh no, we’ll have to add obesity since my oncologist just told me my BMI is higher than 25 and must be lowered in order to keep the possibility of cancer reoccurrence to a minimum.  Then there’s midline incision. My scar runs down the middle of my front from the breasts to below the belly button. Oh, and let’s not forget pre-operative chemotherapy. I had plenty of that. Then there’s intra-operative blood transfusion… to the tune of six for me. I almost forgot to include diabetes mellitus. Hmm, I do believe I had steroid therapy during my chemotherapy treatments, too.

Now what? The hernia is right there, visibly noticeable along the scar line and I understand all the possible reasons it’s there. We all know I have to do something about it, but why? Healthline at https://www.healthline.com/health/hernia#complications answers that question for us.

“Sometimes an untreated hernia can lead to potentially serious complications. Your hernia may grow and cause more symptoms. It may also put too much pressure on nearby tissues, which can cause swelling and pain in the surrounding area.

A portion of your intestine could also become trapped in the abdominal wall. This is called incarceration. Incarceration can obstruct your bowel and cause severe pain, nausea, or constipation.

If the trapped section of your intestines doesn’t get enough blood flow, strangulation occurs. This can cause the intestinal tissue to become infected or die. A strangulated hernia is life-threatening and requires immediate medical care.”

Uh-oh. What can I do? My oncologist suggested a wait and see approach with a twist. I’m now wearing something similar to the belly band that pregnant women wear. The differences are that this is worn around my body to cover the hernia and is very tight in an attempt to have the hernia heal itself. Will this work? That remains to be seen.

What if it doesn’t? Well, there’s always surgery. The National Center for Biotechnology Information (NCBI) at https://bit.ly/3hsFHae tells us,

“The treatment options for incisional hernias are open surgery or minimally invasive surgery. Minimally invasive surgery is also called ‘keyhole surgery,’ or ‘laparoscopic’ surgery if it is performed on the abdomen.”

Wait a minute, laparoscopic surgery. What’s that? Let’s go to MedlinePlus to see what we can find out. This explanation was at https://bit.ly/2RmkS5R.

“Laparoscopic surgery is a surgical technique in which short, narrow tubes (trochars) are inserted into the abdomen through small (less than one centimeter) incisions. Through these trochars, long, narrow instruments are inserted. The surgeon uses these instruments to manipulate, cut, and sew tissue.”

That does seem less invasive, but it’s still surgery. Let’s take a look at recovery time for laparoscopic surgery vs. open surgery. Open surgery is just what it sounds like: you’re cut open.

“When the surgeons are equally skilled and a procedure is available as both an open procedure and a minimally invasive one, the minimally invasive technique almost always offers a lower risk of infection, shorter recovery times and equally successful outcomes.”

Mind you, sometimes keyhole or laparoscopic surgery is not a choice since the surgeon needs to work on a larger area. For example, I had open cancer surgery since not only the tumor, but also my gall bladder and spleen, needed to be removed. Sometimes, what starts out as minimally invasive surgery becomes open surgery when the surgeons run into a problem or realize they need to work on a larger internal area than they’d originally thought.

I still find it amazing how connected all parts of our body are… like Chronic Kidney Disease adding to affecting a scar to the point that a hernia develops.

Until next week,

Keep living your life!

It Isn’t  Ain’t; It’s AIN.  

I’ll explain that in a minute, but first – on this Labor Day weekend – I want to thank all the readers who have liked individual blogs. These likes let me know I’m writing about topics that interest you.

Let’s turn to AIN now.  You know it’s not just a word, but an acronym. That’s a word formed by the initials of a term, like ASAP for as soon as possible. By the way, ‘nym’ means name, while ‘acr’ means height, summit, tip, top.  ‘O’ connects the two roots. So, we have the tip of the words or the first letters forming an acronym which becomes a recognized word. Thank you to my college course in Greek and Latin roots. I knew that would come on handy someday and it has again and again.

Well, what does AIN mean? It is the acronym for Allergic Interstitial Nephritis, which is a mouthful itself. ‘Allergic’ we get. That’s a common enough word. ‘Interstitial’, though? I remember the prefix (group of related words before the root word that changes its meaning) ‘inter’ means between, but between what? Merriam-Webster Dictionary at https://bit.ly/3h3cF0H, here we come.

asituated within but not restricted to or characteristic of a particular organ or tissue —used especially of fibrous tissue

 baffecting the interstitial tissues of an organ or part

I wonder if we’ll need both definitions. I think we need to be reminded of what nephritis is before we can tell. Again, I remember from that college course so very long ago (Funny what sticks in your mind, isn’t it?) that ‘itis’ means inflammation. We know from all the writings about Chronic Kidney Disease that ‘neph’ means kidneys. Putting these together, we have inflammation of the kidneys. Let’s take a look at my favorite dictionary again, just to be certain.

Yep, there we have it at www.merriam-webster/dictionary/nephritis:

“acute or chronic inflammation of the kidney caused by infection, degenerative process, or vascular disease”

How do you define the whole term? According the excerpt from Nancy A. Finnigan and Khalid Bashir’s book Statpearls on NCBI’s bookshelf at https://bit.ly/31ZTeS2,

“Allergic interstitial nephritis (AIN) is the most common form of acute interstitial nephritis. It is most often caused by exposure to a drug. AIN is often associated with an acute decline in renal function and may be associated with permanent renal insufficiency.”

Acute? Oh, yes. That’s means sudden. It’s the opposite of chronic, which means long term. Looks like we only needed the second dictionary definition of interstitial after all.

So, this kind of nephritis is usually caused by drugs? Which drugs? I went to UpToDate at https://bit.ly/3i4exHS for the answer:

“The most common drug causes of AIN now include …:

  • Nonsteroidalanti-inflammatoryagents (NSAIDs), including selective cyclooxygenase (COX)-2 inhibitors
  • Penicillinsand cephalosporins
  • Rifampin
  • Antimicrobial sulfonamides, including trimethoprim-sulfamethoxazole
  • Ciprofloxacin and,perhaps toa lesser degree, other quinolones
  • Diuretics, including loop diuretics such as furosemide and bumetanide, and thiazide-type diuretics
  • Cimetidine (only rare cases have been described with other H-2 blockers such as ranitidine) [24,25]
  • Allopurinol
  • Proton pump inhibitors (PPIs) such as omeprazole and lansoprazole [26-29]
  • Indinavir
  • 5-aminosalicylates (eg, mesalamine)”

There are some very common drugs on this list. As Chronic Kidney Disease patients, we are warned away from NSAIDS. I’ve been warned about Ciprofloxacin, too, and PPIs, but diuretics? Most of the other drugs we’d have to ask our doctors about when and if they’re prescribed. Then again, I ask my family doctor to check the effect of the drug on the kidneys when she prescribes a drug. She happily does so.

You should note that many of these drugs do not require a prescription. In that case, speak with your pharmacist about its possible effect on your kidneys before buying any over the counter drug. Another possibility is using Drugs.com or a similar website for possible effects on your kidneys before using any drugs.

What are the symptoms, if any, of AIN? Well, much like Chronic Kidney Disease, there are often no symptoms until it is quite advanced. Then you would notice the acute drop in kidney function. A blood test and urine test will help with the diagnosis, although the urine test will only show the presence of white blood cells. That indicates an infection. Sometimes a kidney biopsy is required to diagnose AIN.

And now the biggie: what do you do if you develop AIN? You stop the medication. It’s common sense. Your doctor will probably suggest that once it’s been determined you have allergic interstitial nephritis. Remember though, there are other causes of AIN such as infections and/or autoimmunity.

Topic switch: While I’ve been laboring over this blog, I’ve also been thinking about the fact that today is Labor Day in the United States. Coming from a union family, I thought I’d tell you a little bit about Labor Day that you may not know.

This, and more information about Labor Day, may be found at https://bit.ly/3jPeaRR

“In the late 1800s, the state of labor was grim as U.S. workers toiled under bleak conditions: 12 or more hour workdays; hazardous work environments; meager pay. Children, some as young as 5, were often fixtures at plants and factories.

The dismal livelihoods fueled the formation of the country’s first labor unions, which began to organize strikes and protests and pushed employers for better hours and pay. Many of the rallies turned violent.

On Sept. 5, 1882 — a Tuesday — 10,000 workers took unpaid time off to march in a parade from City Hall to Union Square in New York City as a tribute to American workers. Organized by New York’s Central Labor Union, It [sic]was the country’s first unofficial Labor Day parade. Three years later, some city ordinances marked the first government recognition, and legislation soon followed in a number of states.”

As many of you already know, my grandfather was an organizer for the Brass Workers Union. Many a time he’d disappear. He was jailed for his activities, but that didn’t stop him.

As you labor to avoid AIN and keep your kidneys functioning properly, enjoy the holiday weekend.

Until next week,

Keep living your life!

The Dye is Cast

Bet you think I made a spelling error in the title. If you’re thinking of the original phrase, you’re right. In that one, it’s spelled ‘die’. Here’s where it came from according to Wikipedia at https://en.wikipedia.org/wiki/Alea_iacta_est:

Alea iacta est (‘The die has been cast’) is a variation of a Latin phrase (iacta alea est [ˈjakta ˈaːlɛ.a ˈɛst]) attributed by Suetonius to Julius Caesar on January 10, 49 BCE, as he led his army across the Rubicon river in Northern Italy…. The phrase, either in the original Latin or in translation, is used in many languages to indicate that events have passed a point of no return. It is now most commonly cited with the word order changed (‘Alea iacta est’) rather than in the original phrasing….”

Uh-oh, there is in existence a phrase just like the title of today’s blog. It means the tint has been applied and can’t be changed or something like that.That this phrase with this spelling exists was a bit surprising. What I meant in the title is the dye used in contrast CTs.

Let’s back up just a bit so we can explain what a CT is. The Mayo Clinic at https://mayocl.in/3jujqdk tells us:

A computerized tomography (CT) scan combines a series of X-ray images taken from different angles around your body and uses computer processing to create cross-sectional images (slices) of the bones, blood vessels and soft tissues inside your body. CT scan images provide more-detailed information than plain X-rays do.”

I’ll be having one with contrast this afternoon. You know we, as CKD patients, have been warned not to allow that contrast into our bodies. Let’s find out why and then I’ll tell you why I am allowing it. The contrast is the dye in the title of today’s blog.

“In a CT scan, dense substances like bones are easy to see. But soft tissues don’t show up as well. They may look faint in the image. To help them appear clearly, you may need a special dye called a contrast material. They block the X-rays and appear white on the scan, highlighting blood vessels, organs, or other structures.Contrast materials are usually made of iodine or barium sulfate. You might receive these drugs in one or more of three ways:

  • Injection: The drugs are injected directly into a vein. This is done to help your blood vessels, urinary tract, liver, or gallbladder stand out in the image.
  • Orally: Drinking a liquid with the contrast material can enhance scans of your digestive tract, the pathway of food through your body.
  • Enema: If your intestines are being scanned, the contrast material can be inserted in your rectum.

After the CT scan, you’ll need to drink plenty of fluids to help your kidneys remove the contrast material from your body.”Thank you, WebMD at https://www.webmd.com/cancer/what-is-a-ct-scan#2 for the above information.

Of course, now we need to know why we shouldn’t be having this contrast material. Radiology Affiliates Imagining at https://4rai.com/blog/can-contrast-hurt-my-kidneys, a new site for me but one that seems very thorough, explains that we just don’t know for sure:

“…. Unhealthy kidneys, though, may be slower and less efficient when it comes to clearing the contrast from the blood. While the medical community has not yet determined exactly how contrast dye causes kidney problems, they think it has to do with this slow clearance of the dyes from the body.”

Well, what problems can contrast dye cause for our kidneys? I went right to the National Kidney Foundation at https://bit.ly/2YL7RXv  for an answer to this question

“What is Contrast Induced Nephropathy (CIN)?

CIN is a rare disorder and occurs when kidney problems are caused by the use of certain contrast dyes. In most cases contrast dyes used in tests, such as CT (computerized tomography) and angiograms, have no reported problems. About 2 percent of people receiving dyes can develop CIN. However, the risk for CIN can increase for people with diabetes, a history of heart and blood diseases, and chronic kidney disease (CKD)….The risk of CIN in people with both CKD and diabetes is 20 to 50 percent.

CIN is associated with a sharp decrease in kidney function over a period of 48-72 hours. The symptoms can be similar to those of kidney disease, which include feeling more tired, poor appetite, swelling in the feet and ankles, puffiness around the eyes, or dry and itchy skin. In many cases, CIN is reversible and people can recover. However, in some cases, CIN can lead to more serious kidney problems and possible heart and blood vessel problems

What is Nephrogenic Systemic Fibrosis (NSF)?

NSF is a rare but serious disease affecting skin and other organs that has been found in some patients with advanced CKD after exposure to gadolinium-containing contrast dyes that are used in magnetic resonance imaging (MRI). NSF appears to affect about 4 percent of patients with advanced CKD. People with acute kidney injury (AKI) are also at higher risk. NSF has not been reported in people with mild kidney damage or normal kidney function.

NSF can be painful, debilitating, or even fatal. Symptoms and signs of NSF can include burning and itching of the skin, red or dark patches on the skin, joint stiffness, or muscle weakness. The disease can develop within 24 hours up to around 3 months….  delay in excretion [of this drug] is thought to be one the main reasons why NSF may happen.”

Notice that both possible effects of using contrast dye with kidney disease are rare.

So why am I having the contrast dye when I’ve been advised not to? My oncology team needs to see if the cancer has returned and, if it has, how badly. I told them at the beginning of my treatment to spare my kidneys as much as possible. But, in this case, I don’t want them to spare my kidneys so much that I end up dead of cancer.

There are two kinds of dye used, one less harmful to the kidneys than the other. I believe that’s the one that is used on me. It is also reduced in order to save me from any possible further kidney damage. Most importantly, my creatinine level is measured before administering the contrast dye. After a year and a half of this, my kidneys are doing just as well as they were doing before I started allowing contrast dye.

This is my story; remember, everyone is different and talk this over with your nephrologist before you agree to contrast dye. My nephrologist and I agreed that I needed to be alive more than I needed to save my kidneys.

Until next week,

Keep living your life!

Not Your New Age Crystals 

I was perusing the Facebook Chronic Kidney Disease online support groups as I usually do in the morning when I ran across a post that caught my eye. The person posting wanted to know if he were going to die because he had crystals in his urine. I’d never thought about that before. He sounded really scared, so I decided to take a look at this condition.

First of all, some basic information from Study.com at https://bit.ly/34n3W6H:

“Crystals in the urine is known as crystalluria. Sometimes crystals are found in healthy people and other times they are indicators of organ dysfunction, the presence of urinary tract stones of a like composition (known as urolithiasis), or an infection in the urinary tract.”

Ummm, I wanted a bit more information so I turned to Healthline.com at https://www.healthline.com/health/urine-crystals.

“Crystals can be found in the urine of healthy individuals. They may be caused by minor issues like a slight excess of protein or vitamin C. Many types of urine crystals are relatively harmless.

In some cases, however, urine crystals can be indicators of a more serious underlying condition. Symptoms that would indicate a more serious condition could include:

  • fever
  • severe abdominal pain
  • blood in the urine
  • jaundice
  • Fatigue”

Serious conditions? What does that mean? The organ dysfunction Study.com mentioned? Which organs? Urolithiasis? An infection? Can you die from any of these?

Time to slow down. Since this is a Chronic Kidney Disease blog, let’s start with the kidneys.

“Crystal-induced acute kidney injury (AKI) is caused by the intratubular precipitation of crystals, which results in obstruction. Crystal-induced AKI most commonly occurs as a result of acute uric acid nephropathy and following the administration of drugs or toxins that are poorly soluble or have metabolites that are poorly soluble in urine …. Other drugs or medications may be metabolized to insoluble products such as oxalate (ethylene glycol, vitamin C), which are associated with precipitation of calcium oxalate crystals within tubular lumens and kidney injury.”

Thank you UptoDate.com at https://bit.ly/3j3BT0k for this information, although we’ll need some explanation in order to understand it. I get it that crystals can produce obstruction in the tubules (Wikipedia: The renal tubule is the portion of the nephron containing the tubular fluid filtered through the glomerulus), rather than being passed out of the body in the urine. It makes sense that if the crystals do produce obstruction, the urine may back up… right into the kidneys. That’s when you have the AKI. Remember, this in not chronic. The condition remains until it’s remedied, but it can be remedied.

What about urolithiasis? I must thank the National Kidney Foundation at https://www.kidney.org/atoz/content/hydronephrosis for their easily understood information about a condition called hydronephrosis which will explain how both urolithiasis and/or an infection would affect your kidneys.

“Hydronephrosis is the swelling of a kidney due to a build-up of urine. It happens when urine cannot drain out from the kidney to the bladder from a blockage or obstruction. (Gail here: such as the blockage caused by crystals which results in AKI.) Hydronephrosis can occur in one or both kidneys.

The main function of the urinary tract is to remove wastes and fluid from the body. The urinary tract has four parts: the kidneys, the ureters, the bladder and urethra. The urine is formed when the kidneys filter blood and remove excess waste materials and fluid. Urine collects into a part of the kidney called the renal pelvis. From the renal pelvis, the urine travels down a narrow tube called the ureter into the bladder. The bladder slowly fills up with urine, which empties from the body through another small tube called the urethra. Hydronephrosis occurs when there is either a blockage of the outflow of urine, or reverse flow of urine already in the bladder (called reflux) that can cause the renal pelvis to become enlarged.

Hydronephrosis may or may not cause symptoms. The main symptom is pain, either in the side and back (known as flank pain), abdomen or groin. Other symptoms can include pain during urination, other problems with urination (increased urge or frequency, incomplete urination, incontinence), nausea and fever. These symptoms depend on the cause and severity of urinary blockage.

How is Hydronephrosis Caused?
Hydronephrosis is usually caused by another underlying illness or risk factor. Causes of hydronephrosis include, but are not limited to, the following illnesses or risk factors:

  • Kidney stone
  • Congenital blockage (a defect that is present at birth)
  • Blood clot
  • Scarring of tissue (from injury or previous surgery)
  • Tumor or cancer (examples include bladder, cervical, colon, or prostate)
  • Enlarged prostate (noncancerous)
  • Pregnancy
  • Urinary tract infection (or other diseases that cause inflammation of the urinary tract)”

Kidney stones? MedicalNewsToday at https://www.medicalnewstoday.com/articles/154193 helped us out with that one:

“Kidney stones are the result of a buildup of dissolved minerals on the inner lining of the kidneys.

They usually consist of calcium oxalate but may be composed of several other compounds.

Kidney stones can grow to the size of a golf ball while maintaining a sharp, crystalline structure.

The stones may be small and pass unnoticed through the urinary tract, but they can also cause extreme pain as they leave the body.”

There is quite a bit more information about kidneys stones at this site. What we needed to know is that, again, it’s a buildup – as in not passed from the body via the urine – that causes kidney stones.

Will the person who posted the comment about crystals in his urine die, whether or not he develops symptoms? It seems to me that’s not necessary IF he seeks treatment and follows medical advice.

Back to Healthline, but this time at https://www.healthline.com/health/urine-crystals#prevention, for their take on this question:

“Urine crystals that aren’t caused by underlying conditions like liver disease or genetic conditions can often be prevented. In some cases, even crystalluria triggered by genetic causes can be reduced with lifestyle or diet changes.

The most effective way to prevent urine crystals is to drink more water and stay hydrated. This helps dilute the chemical concentrations in the urine, preventing crystals from forming.

You can also make certain changes in your diet. Your doctor can help you determine what changes to make based on the type of crystals that you have. They may recommend cutting back on protein, for example, or reducing foods high in oxalate (as is the case for calcium oxalate crystals).

Avoiding salty foods can also help prevent a number of different urine crystals, so eliminating processed foods can be beneficial.”

I’m going to add today’s blog to the things-I-never-knew part of my brain.

Until next week,

Keep living your life!

I’ve Been Compromised 

It’s true, and it’s not only me. It’s you, too, if you have Chronic Kidney Disease. ‘What do I mean?’ you ask. It’s your immune system that’s been compromised by your CKD. ‘HOW?’ you demand. That’s what today’s blog is going to explain.

Let’s start the usual way: at the beginning. 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 at https://medlineplus.gov/immunesystemanddisorders.html

“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.”

According to the National Kidney Foundation at https://www.kidney.org/atoz/chronic-kidney-disease-and-pneumococcal-disease-do-you-know-facts,

“…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.”

That makes sense. But exactly how does CKD compromise this system?

According to a British Society for Immunology study published in PubMed [“PubMed Central (PMC) is a free archive of biomedical and life sciences journal literature at the U.S. National Institutes of Health’s National Library of Medicine (NIH/NLM),” as stated on their website. NCBI is The National Center for Biotechnology Information.] at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5904695/:

“The immune system and the kidneys are closely linked. In health the kidneys contribute to immune homeostasis, while components of the immune system mediate many acute forms of renal disease and play a central role in progression of chronic kidney disease. A dysregulated immune system can have either direct or indirect renal effects. Direct immune‐mediated kidney diseases are usually a consequence of autoantibodies directed against a constituent renal antigen, …. Indirect immune‐mediated renal disease often follows systemic autoimmunity with immune complex formation, but can also be due to uncontrolled activation of the complement pathways. Although the range of mechanisms of immune dysregulation leading to renal disease is broad, the pathways leading to injury are similar. Loss of immune homeostasis in renal disease results in perpetual immune cell recruitment and worsening damage to the kidney. Uncoordinated attempts at tissue repair, after immune‐mediated disease or non‐immune mediated injury, result in fibrosis of structures important for renal function, leading eventually to kidney failure.”

Hmmm, it seems my linking function is not working for this URL. No loss, just copy and paste the URL if you’d like to read more about the immune system and the kidneys.

There are a few medical terms in the above paragraph that you may need defined. Thank you, my all-time favorite dictionary, the Merriam-Webster, for helping us out here.

Antibodyany of a large number of proteins of high molecular weight that are produced normally by specialized B cells after stimulation by an antigen and act specifically against the antigen in an immune response, that are produced abnormally by some cancer cells, and that typically consist of four subunits including two heavy chains and two light chains

(https://www.merriam-webster.com/dictionary/antibody)

Antigenany substance (such as an immunogen or a hapten [Gail here: Bing defines this as “a small molecule which, when combined with a larger carrier such as a protein, can elicit the production of antibodies which bind specifically to it (in the free or combined state.]) foreign to the body that evokes an immune response either alone or after forming a complex with a larger molecule (such as a protein) and that is capable of binding with a product (such as an antibody or T cell) of the immune response

(https://www.merriam-webster.com/dictionary/antigen)

Autoantibodiesan antibody active against a tissue constituent of the individual producing it

(https://www.merriam-webster.com/dictionary/autoantibodies)

Fibrosisa condition marked by increase of interstitial fibrous tissue [Gail here: That’s not much help. In a word, fibrosis means scarring.]

(https://www.merriam-webster.com/dictionary/fibrosis)

Renal: of, relating to, involving, or located in the region of the kidneys

(https://www.merriam-webster.com/dictionary/renal)

Oh, boy. Now what? Can we build up our immune system? WebMD’s slide show  at https://www.webmd.com/diet/ss/slideshow-strengthen-immunity offers some ways we can. To summarize this slide show:

  1. Avoid stress.
  2. Have sex more often (I love this one.)
  3. Get a pet.
  4. Be optimistic.
  5. Build your social network
  6. Laugh more.
  7. Eat colorful fruits and vegetables. (Within your kidney diet, of course.)
  8. Consider herbs and supplements. (Check with your nephrologist first.)
  9. Exercise.
  10. Sleep an adequate number of hours.
  11. Cut back on alcohol consumption.
  12. Stop smoking.
  13. Keep washing those hands.

Some doctors, such as  Dr. Suzanne Cassel, an immunologist at Cedars-Sinai, think we need to balance our immune systems rather than strengthen them. ” ‘You actually don’t want your immune system to be stronger, you want it to be balanced,’ Dr. Cassel says. ‘Too much of an immune response is just as bad as too little response.’

Dr. Cassel says most of the things people take to boost their immune system, such as vitamins or supplements, don’t have any effect on your immune response.”

Obviously, all doctors don’t agree. Whether you want to balance your immune system or strengthen it, the suggestions above will be helpful. Notice whether or not we’re in the middle of a pandemic, washing your hands frequently can help your immune system. Most of the suggestions from WebMD may be surprising to you since they are lifestyle changes and/or are the same ones suggested in general for CKD patients. There’s got to be something to them if they can both help with your CKD and your immune system. Why not try the suggestions you’re not already adhering to?

By the way, to the reader who asked why chocolate is not good for CKD patients, it’s loaded with potassium. In addition, many CKD patients also have diabetes. The sugar content in chocolate is not going to do them any good.

Until next week,

Keep living your life!

Getting Ready  

As I mentioned last week, I am lucky enough to be cancer free now and have returned to my other specialists. But we are experiencing the Covid-19 pandemic which means most of my doctors are conducting telemedicine appointments.

What are those? Let’s go to my favorite dictionary, The Merriam-Webster Dictionary, and see what we can see. I found this at https://www.merriam-webster.com/dictionary/telemedicine:

“the practice of medicine when the doctor and patient are widely separated using two-way voice and visual communication (as by satellite or computer)”

Surprisingly, I also discovered this has been in use since 1968. Maybe that’s why the phone and/or iPad type devices weren’t mentioned in the definition.

Of course, if you need to be examined physically, you’ll have to go to the doctor’s office. For example, poor Bear needed several mole biopsies last week. Obviously, he had to present himself at his dermatologist’s office to have these procedures carried out.

But I’ve been fortunate to be able to stick with telemedicine. Yet, you’ve got to be prepared for such doctor appointments. Do you have a thermometer? You’ll be asked for your temperature. We use both the DTT (digital temple thermometer) and Target’s talking thermometer (for those days when neither of us can find our glasses… really.) It seems the DTT we use is no longer manufactured, but the updated one is only about $15.00. The talking ear digital thermometer is more expensive. That one runs about double the price of the DTT. I did discover that digital mouth thermometers can be as low as $8.00. Non-digital oral thermometers start at about $6.00 You can compare prices online for the best deal. However, we are apparently old fashioned. The newest form of temperature assessment is the no contact digital scan thermometer. This one starts at about $50.

So, you have your temperature reading ready. What else will you need? I’ve always been asked for my blood pressure and pulse. I use an arm, rather than a wrist, device since my family doctor explained to me that the wrist device takes a reading through two bones. Those are the radius and ulna. The arm device takes your reading through only one bone, the humerus. She feels a reading through only one bone is more accurate. What device do I use? No matter which ones I’ve experimented with, I always return to Omron. It’s easy to use and accurate. These run from about $33 to over $100, depending upon how fancy you want to go. This description is from Amazon’s mid-price Omron:

Platinum (new version)

  • Trusted brand – Omron is the #1 recommended home blood pressure monitor brand by doctors and pharmacists for clinically-accurate home monitoring, and the #1 selling manufacturer of home blood pressure monitors for over 40 years.
  • Unlimited memory and users with the free app – The Omron gold wrist monitor stores 200 total blood pressure readings for 2 users (100 per user, most of any Omron wrist blood pressure monitor). Memory and users are unlimited with the Omron connect free app which works with amazon alexa-enabled devices (on select IOS & android devices).
  • High morning average indicator – Among Omron Amazon-exclusive blood pressure monitors, this feature is unique to the Gold and Platinum monitors. The indicator alerts the user if systolic or diastolic measurements are out of normal range in the morning, when there is a higher risk for heart attack or stroke.
  • Dual display with backlight – The Omron Platinum monitor features a backlit dual-display LCD monitor with easy navigation that allows the user to immediately compare the current reading to the previous reading. The backlight feature is only available with the Platinum Monitor.
  • AC adapter included – The Omron Ac Adapter eliminates the worry of changing batteries in your Omron Blood Pressure Monitor. The convenient AC adapter helps make sure your monitor is ready whenever you are.”

What else now? Let me think for a minute. Of course, if you are prediabetic or diabetic, you’ll be asked for your latest blood sugar readings. Believe it or not, I prefer WalMart’s no nonsense, no frills ReliOn Prime blood glucose monitor. In case you didn’t know, WalMart also operates as Sam’s Club. For my non-U.S.A. readers, according to https://en.wikipedia.org/wiki/Walmart, Walmart International operates in these countries:

Let’s keep in mind that anyone can edit in Wikipedia, so be certain to check before you bank upon going.

My family doctor did prescribe another brand which is a bit fancier in that it has a nicer looking case, lancet ejector, and meter. It was also more expensive and a prescription was needed.

If this is all new to you, you need to know you not only need this kit (which contains the monitor, a lancing device for your lancets, and spaces to store both your test strips and needles), but also the afore mentioned test strips and lancing device. You can buy 100 ultra-thin lancets for under $3.00. I suggest ultra-thin because I’ve found the thinner the lancet, the less the poke to get that one drop of blood needed for testing hurts.

The test strips are another story. These are expensive. They usually cost a little less than $18.00 for 100. And the lancing device? That’s about $6.00. The monitor itself is $9.00. The case comes with your starter kit. I haven’t found one sold separately by Walmart, although Amazon has a few for other brands. The number of times you need to test your blood glucose daily determines the weekly cost of your supplies.

You’ll also be asked for your height and weight. I have to admit I’m partial to digital devices and so have a digital scale from Amazon. Their scales run from $18.00 to $35.00. Of course, non-digital will be less expensive.

As for the height, I guess I cheated. I looked up the most recent height recorded on my last doctor’s appointment and used that.

Conclusion: You’ll need your temperature, blood pressure, height, weight, – if you’re prediabetic or diabetic – your blood glucose, and a phone, iPad sort of device, or computer for your telemedicine appointment.  Now you’re ready.

May you only have good results.

Until next week,

Keep living your life!

I Can’t Eat That 

Now that I’m cancer free, I’ve resumed visits to all the other specialists (Isn’t growing older wonderful?) I had been seeing before the cancer diagnosis. One of these specialists was my immunologist, who had suggested I stop taking my allergy injections while I was doing chemotherapy since the chemo would change many of the conditions in my body. She was right. I no longer need the monthly injections for seasonal allergies, but there are certain foods I can no longer eat.

Why not, you may be asking yourself. Easy answer? I’m allergic to them. Wait just a minute here. What exactly does allergic mean and how will this affect your Chronic Kidney Disease?

The Merriam-Webster dictionary at https://www.merriam-webster.com/dictionary/allergy tells us that allergy means,

“1altered bodily reactivity (such as hypersensitivity) to an antigen in response to a first exposure….

2exaggerated or pathological immunological reaction (as by sneezing, difficult breathing, itching, or skin rashes) to substances, situations, or physical states that are without comparable effect on the average individual

3medical practice concerned with allergies

4a feeling of antipathy or aversion”

It’s definition number two for us. Maybe an explanation of those monthly allergy injections would be helpful here, too. The Mayo Clinic at https://www.mayoclinic.org/tests-procedures/allergy-shots/about/pac-20392876#:~:text=If%20you%20get%20weekly%20or,reaction%2C%20particularly%20a%20local%20reaction had the explanation we needed:

“Allergy shots are regular injections over a period of time — generally around three to five years — to stop or reduce allergy attacks. Allergy shots are a form of treatment called immunotherapy. [Gail here: Hence, the specialist who treats allergies is called an immunologist.] Each allergy shot contains a tiny amount of the specific substance or substances that trigger your allergic reactions. These are called allergens. Allergy shots contain just enough allergens to stimulate your immune system — but not enough to cause a full-blown allergic reaction.

Over time, your doctor increases the dose of allergens in each of your allergy shots. This helps get your body used to the allergens (desensitization). Your immune system builds up a tolerance to the allergens, causing your allergy symptoms to diminish over time.”

Lucky me: no more seasonal allergies. Let’s get back to those food allergies and CKD now… or not. While I found quite a bit of information about drug allergies, I found very little about food allergies. It’s nice to know my allergies to shellfish and vanilla will not harm my kidneys. Come to think of it, I don’t eat these foods because I’m allergic to them, so they’re not in my system anyway.

Hmmm, is it any different with food sensitivities? How’s about a definition first. It’s so nice to have a favorite dictionary. This is what The Merriam-Webster Dictionary at https://www.merriam-webster.com/dictionary/sensitivity?utm_campaign=sd&utm_medium=serp&utm_source=jsonld has to say:

“the quality or state of being sensitive: such as

athe capacity of an organism or sense organ to respond to stimulation: IRRITABILITY

bthe quality or state of being hypersensitive

cthe degree to which a radio receiving set responds to incoming waves

dthe capacity of being easily hurt

eawareness of the needs and emotions of others”

Definition a is the one we need.

Again, I did not find enough validation that food sensitivities could damage our kidneys to write about it.

Maybe I’m looking at this backwards. Maybe it’s not do food sensitivities and allergies damage our kidneys that I should be dealing with, but rather can they cause kidney damage. Back to the internet. Will you look at that? Again, there was much more information about drug allergies damaging your kidneys and very little about food allergies or sensitivities.

I’ve satisfied myself that, just as with my food allergies, my sensitivity to lactose, wheat, fructose syrup, and acidic foods will not harm my kidneys. Although, they may cause me to read more food labels than I usually do. Hopefully, you’re satisfied that your food allergies and sensitivities will not harm your kidneys. If you’re still concerned, speak with your nephrologist or renal dietitian.

Of course, none of this means we can ignore the kidney diet. That is, not if you want to slow down the progression of the decline of your kidney function. Eat according to your labs. Keep watching your potassium, phosphorous, protein, and sodium restrictions. This is highly individualized, so again: speak with your nephrologist or renal dietitian should you have questions.

While we’re on the subject of food, do you remember when I wrote about Flavis? That’s the low sodium, low phosphorus, low potassium food company. Bear made a beef stew which we decided to eat upon a layer of pasta. We chose Flavis’s fusilli. That’s a kind of short, spiral pasta. I have got to say it was delicious. I like that it tastes so light, especially since I usually find pasta so heavy.   

News! I’ve gotten so many emails asking where readers can buy my books that I’ve made each title clickable. Click on the title and you go directly to the book’s page on Amazon.com. The titles are to the right of the blog itself on the blog roll.

I know, especially now in the time of Covid-19, that money can be an issue and even the $2.99 for the digital version of each of the books can be $2.99 too much. In that case, I suggest you request your library order the book and then you can borrow it for free. Even libraries that have shut down have virtual sites now. I do humbly request reviews from those of you who read the books. You can leave them on the Amazon.com page for each book. Thank you in advance.

Until next week,

Keep living your life!

Balloon sans Cake or Ice Cream

I am at Stage 3A, which is still pretty far from dialysis or End Stage Kidney Disease (ESRD) which is usually Stage 5. Chronic Kidney Disease (CKD) is staged by your Glomerular Filtration Rate (GFR). This graphic will make it clear.

I don’t know very much about dialysis. However, I have heard of a fistula. I went to MedlinePlus, which is subdivision of the U.S. National Library of Medicine which, in turn, is a subdivision of the National Institutes of Health at https://medlineplus.gov/ency/article/002365.htm for a formal definition of fistula.

“A fistula is an abnormal connection between two body parts, such as an organ or blood vessel and another structure. Fistulas are usually the result of an injury or surgery. Infection or inflammation can also cause a fistula to form.

Information

Fistulas may occur in many parts of the body. They can form between:

  • An artery and vein
  • Bile ducts and the surface of the skin (from gallbladder surgery)
  • The cervix and vagina
  • The neck and throat
  • The space inside the skull and nasal sinus
  • The bowel and vagina
  • The colon and surface of the body, causing feces to exit through an opening other than the anus
  • The stomach and surface of the skin
  • The uterus and peritoneal cavity (the space between the walls of the abdomen and internal organs)
  • An artery and vein in the lungs (results in blood not picking up enough oxygen in the lungs)
  • The navel and gut”

Now, look again at the first words in the list above: “an artery and vein.” That’s the way fistulas for dialysis are formed. But how?

“A vascular access is a hemodialysis patient’s lifeline, because it makes life-saving hemodialysis treatments possible. Hemodialysis is a treatment for kidney failure that uses a machine to send the patient’s blood through a filter, called a dialyzer, outside the body. The access is a surgically created vein used to remove and return blood during hemodialysis. The blood goes through a needle, a few ounces at a time. The blood then travels through a tube that takes it to the dialyzer. Inside the dialyzer, the blood flows through thin fibers that filter out wastes and extra fluid. The machine returns the filtered blood to the body through a different tube. A vascular access lets large amounts of blood flow continuously during hemodialysis treatments to filter as much blood as possible per treatment. About a pint of blood flows through the machine every minute. A vascular access should be in place weeks or months before the first hemodialysis treatment.”

Thank you to the University of California, San Francisco, Department of Surgery at https://surgery.ucsf.edu/conditions–procedures/vascular-access-for-hemodialysis.aspx for even more useful information than I’d sought.

But now we need to know what hemodialysis is. The National Kidney Foundation at https://www.kidney.org/atoz/content/hemodialysis was a fount of knowledge for us (as it always is):

“When is dialysis needed?

You need dialysis if your kidneys no longer remove enough wastes and fluid from your blood to keep you healthy. This usually happens when you have only 10 to 15 percent of your kidney function left. [Gail here: that’s stage 5 or ESRD.] You may have symptoms such as nausea, vomiting, swelling and fatigue. However, even if you don’t have these symptoms yet, you can still have a high level of wastes in your blood that may be toxic to your body. Your doctor is the best person to tell you when you should start dialysis.

How does hemodialysis work?

Hemodialysis is a procedure where a dialysis machine and a special filter called an artificial kidney, or a dialyzer, are used to clean your blood. To get your blood into the dialyzer, the doctor needs to make an access, or entrance, into your blood vessels. This is done with minor surgery, usually to your arm. ….

How does the dialyzer clean my blood?

The dialyzer, or filter, has two parts, one for your blood and one for a washing fluid called dialysate. A thin membrane separates these two parts. Blood cells, protein and other important things remain in your blood because they are too big to pass through the membrane. Smaller waste products in the blood, such as urea, creatinine, potassium and extra fluid pass through the membrane and are washed away.”

By the way, hemodialysis is not the only kind of dialysis.

Got it? So what’s this about balloon? By this point, you’ve realized it’s not the kind you see at birthday parties as you see cake and ice cream. Someone I know is having this procedure. While talking it over, we realized neither of us knew how it was done or, on some levels, why it was even done. I decided we could both learn about it if I wrote about ballooning.

Well, will you look at that? Ballooning is really angioplasty. The Encarta Dictionary defines angioplasty as,

“a surgical operation to clear a narrowed or blocked artery”

That makes sense since a fistula connects an artery and a vein.

Let’s find out why how it’s done. I found a good explanation from Azura Vascular Care at https://www.azuravascularcare.com/infodialysisaccess/angioplasty-can-help-with-dialysis-access-complications/.

“An angioplasty is a way to fix a blood vessel that has become narrow.

  • If you need an angioplasty, an inflatable balloon will be inserted through the catheter.
  • The balloon is inflated where the narrowing is.
  • You may feel some discomfort when the balloon is inflated.
  • The angioplasty usually takes about 1 hour.
  • One stitch may be placed at the insertion site.
  • The stitch can be taken out the following morning or at your next dialysis treatment.”

Apparently, your artery can be too narrow before you start dialysis. Notice, the person I was speaking with has a fistula, not a catheter. The procedure is the same, except that the balloon is inserted via the fistula.

Well, what about after the angioplasty? This is from the Texas Heart Institute at https://www.texasheart.org/heart-health/heart-information-center/topics/vascular-access-for-hemodialysis/:

“Patients should avoid heavy lifting. Any injury to your arm can cause bleeding. When you go to the doctor, do not let anyone take your blood pressure, start an IV, or take blood from the arm with the A-V fistula or graft.”

Now I know, and so does the person I was speaking with… and so do you.

Until next week,

Keep living your life!

We Know They Do, But How?

  • “aluminum- and calcium-containing antacids
  • anticonvulsants
  • calcium channel blockers
  • diuretics
  • iron supplements
  • narcotic pain medications
  • medicines used to treat Parkinson’s disease”

I ask you what do these drugs have in common. Healthline at https://www.healthline.com/health/what-does-constipation-feel-like#takeaway tells us they all may cause constipation.

This is one of those topics we don’t like to talk about, but have probably each experienced at one time or another. There are other causes of constipation, but today, we’ll stick with that caused by drugs. Mind you, we’re not talking about party drugs. Rather, it’s the drugs that are prescribed for you that may cause constipation which I’m writing about.

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”

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).”

Let’s see if we can get more specific information on how constipation works. I went to Medscape at https://emedicine.medscape.com/article/184704-overview#a4 and discovered there are quite a few different kinds of constipation:

“The etiology [Gail here. That means the cause of the disease.] of constipation is usually multifactorial, but it can be broadly divided into two main groups …: primary constipation and secondary constipation.

Primary constipation

Primary (idiopathic, functional) constipation can generally be subdivided into the following three types:

Normal-transit constipation (NTC)

Slow-transit constipation (STC)

Pelvic floor dysfunction (ie, pelvic floor dyssynergia)

NTC is the most common subtype of primary constipation. Although the stool passes through the colon at a normal rate, patients find it difficult to evacuate their bowels. Patients in this category sometimes meet the criteria for IBS with constipation (IBS-C). The primary difference between chronic constipation and IBS-C is the prominence of abdominal pain or discomfort in IBS. Patients with NTC usually have a normal physical examination.

STC is characterized by infrequent bowel movements, decreased urgency, or straining to defecate. It occurs more commonly in female patients. Patients with STC have impaired phasic colonic motor activity. They may demonstrate mild abdominal distention or palpable stool in the sigmoid colon.

Pelvic floor dysfunction is characterized by dysfunction of the pelvic floor or anal sphincter. Patients often report prolonged or excessive straining, a feeling of incomplete evacuation, or the use of perineal or vaginal pressure during defecation to allow the passage of stool, or they may report digital evacuation of stool.”

We won’t be dealing with secondary constipation today since that doesn’t include drugs in its etiology.

What does happen 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.”

Imagine, drugs to improve your health taxing your health. Luckily, since you need to take the prescribed drugs to alleviate whatever your medical diagnosis is, there are methods to relieve your constipation. Here’s WebMD’s (https://www.webmd.com/digestive-disorders/constipation-relief-tips) advice:

“One way to keep things moving is by getting enough fiber in your diet, which makes stool bulkier and softer so it’s easier to pass. Gradually increase the amount of fiber in your diet until you’re getting at least 20 to 35 grams of fiber daily.

Good fiber sources include:

  • Bran and other whole grains found in cereals, breads, and brown rice
  • Vegetables such as Brussels sprouts, carrots, and asparagus
  • Fresh fruits, or dried fruits such as raisins, apricots, and prunes”
  • Beans

While you’re having an issue with constipation, limit foods that are high in fat and low in fiber, like cheese and other dairy products, processed foods, and meat. They can make constipation worse.

And on the subject of diet, water is important for preventing constipation, too. Try to drink at least 8 glasses of water a day.

Also, exercise regularly. Moving your body will keep your bowels moving, too.”

Wait a minute. We’re Chronic Kidney Disease patients. That’s means some of the foods listed above may not be allowed on our renal diets. For instance, dried raisin, apricots, and prunes are too high in potassium for CKD patients. You need to speak with your renal dietitian before changing your diet.

As Benjamin Franklin stated, “an ounce of prevention is worth a pound of cure.” Let’s see what we can find on prevention.

  • Increasing your fiber intake: Fiber-rich foods, such as fruits, vegetables and whole grains, all help improve gut function. If you have bowel sensitivity, you’ll want to avoid high-fructose fruits, such as apples, pears and watermelon, which can cause gas.
  • Getting more exercise: Regular exercise can help keep stool moving through the colon.
  • Drinking more water: Aim for eight glasses daily, and avoid caffeine, as it can be dehydrating.
  • Go when you feel like it: When you feel the urge to go, don’t wait.”

Thank you to Johns Hopkins Medicine at https://www.hopkinsmedicine.org/health/conditions-and-diseases/constipation-causes-and-prevention-tips for this information. Will you look at that? Prevention methods for constipation are almost the same as how to treat constipation. Better get started, folks.

Until next week,

Keep living your life!

It’s Time  

Time for what, you ask. Time to talk about Covid-19 and your kidneys. I don’t really want to, and maybe you don’t, either. But this is a pandemic, so we must. Better to know than play ostrich.

By the way, my favorite dictionary, the Merriam Webster at https://www.merriam-webster.com/dictionary/pandemic defines pandemic this way:

pandemic  adjective(Entry 1 of 2)

occurring over a wide geographic area and affecting an exceptionally high proportion of the population 

…..

pandemic noun (Entry 2 of 2)

an outbreak of a disease that occurs over a wide geographic area and affects an exceptionally high proportion of the populationa pandemic outbreak of a disease”

So much is unknown about the current pandemic, but it does look like Covid-19 lends itself to AKI (Acute Kidney Injury).

Let’s go back to this 1918 flu and see if we can find any kidney involvement there. I did, sort of. This study was published by Craig Garthwaite of the Department of Economics at the University of Maryland: The Effect of In-Utero Conditions on Long Term Health: Evidence from the 1918 Spanish Flu Pandemic. It deals with children of mothers who were pregnant during the 1918 Pandemic. You can find it at https://www.kellogg.northwestern.edu/faculty/garthwaite/htm/fetal_stress_garthwaite_053008.pdf.

“Depending on the period of fetal development during which exposure occurred, individuals have a higher probability of developing coronary heart disease, diabetes, kidney disorders, or being in poor health…. When flu exposure is defined using particular quarters of birth, however, there is an approximately 23 percent increase in the probability of developing diabetes for individuals exposed to the flu during the first months of pregnancy.”

Diabetes is the number one cause of Chronic Kidney Disease (CKD). CKD is a kidney disorder.

Did you know that there were three other pandemics between the one in 1918 and today’s? I didn’t. According to the Centers for Disease Control and Prevention (CDC) at https://www.cdc.gov/flu/pandemic-resources/basics/past-pandemics.html, they are

1957-1958 Pandemic (H2N2 virus) “The estimated number of deaths was 1.1 million worldwide and 116,000 in the United States.”

1968 Pandemic (H3N2 virus) “The estimated number of deaths was 1 million worldwide and about 100,000 in the United States.”

2009 H1N1 Pandemic (H1N1pdm09 virus) “… 12,469 deaths … in the United States…. Additionally, CDC estimated that 151,700-575,400 people worldwide died … during the first year the virus circulated.”

While these may seem like scary numbers, as of this past Saturday (and we know these numbers change daily), the World Health Organization (WHO) posted the following numbers:

“Total (new cases in last 24 hours)

Globally 12 322 395 cases (219 983) 556 335 deaths (5 286)”

You can check more data from WHO at https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200711-covid-19-sitrep-173.pdf?sfvrsn=949920b4_2.

The United States statistics?

“Coronavirus Cases:

3,355,646

Deaths:

137,403”

This is according to Worldometers at https://www.worldometers.info/coronavirus/country/us/.

It’s clear the pandemic is not done with us yet. People speak of the second wave coming. I live in Arizona and believe we are still in the first wave. I have no scientific proof for my belief, but our numbers keep going up without ever having gone down.

The National Kidney Foundation at https://www.kidney.org/coronavirus/covid-19-information#can-covid-19-cause-kidney-failure-otherwise-healthy-adults gives us the insight we need into Covid-19 and our kidneys:

“Initial reports from Wuhan found approximately 3% to 9% of hospitalized patients with confirmed COVID-19 developed an AKI. Incidence rates have now increased to 15% of hospitalized patients and 20% and higher in ICU patients with many requiring dialysis treatments. AKI appears to be a marker of COVID-19 infection severity and the mortality rate is higher for these patients.

Various COVID-19-related effects that are thought to contribute to AKI include kidney tubular injury (acute tubular necrosis) with septic shock, microinflammation, increased blood clotting, and probable direct infection of the kidney. Most patients with COVID-19-related AKI who recover continue to have low kidney function after discharge from the hospital.”

As usual, we need to back up a little here. AKI in not CKD (Here we are back in alphabet city.), although it may lead to CKD. While it may raise the death rate of Covid-19 patients, not all Intensive Care Unit (ICU) patients and those with Covid-19 but not in the ICU develop AKI.

Acute tubular necrosis may be a new term for you. Healthline at https://www.healthline.com/health/acute-tubular-necrosis explains it for lay folks like you and me:

“Inside your kidneys are small tube-shaped structures that remove salt, excess fluids, and waste products from your blood. When these tubules are damaged or destroyed, you develop acute tubular necrosis (ATN), a type of acute kidney injury. The damage may result in acute kidney failure.”

This past weekend I received this invitation from the American Association of Kidney Patients (AAKP) and George Washington University which you may find useful for yourself:

“Over the course of the past three months, you’ve joined AAKP and some of our allied experts in one of our nine COVID-19 webinars.

(Gail here: Go to their webinars. They’re a good way to read more about Covid-19 and your kidneys.)

We’re now pleased to invite you to pre-register to join our 2nd Annual Global Summit entitled, Global Kidney Innovations – Expanding Patient Choices & Outcomes, hosted in partnership with the George Washington University School of Medicine and Health Sciences.

This year’s summit focuses on the impact of COVID-19 on kidneys and kidney patients (Gail again: I purposely italicized that part of this sentence.) as well as key innovations in kidney care. All registration fees have been dropped to allow the broadest possible audience of frontline medical professionals, researchers, and kidney patients.

Join us for immediate access to key insights related to COVID-19 and risks to kidney patients! Beyond COVID-19, the agenda focuses on emerging innovation and research to care for kidney diseases, including diversity in clinical trials; precision medicine; genetic conditions such as APOL1; emerging research in the areas of early disease diagnosis and artificial intelligence; novel therapies in transplantation including wearable and artificial implantable devices; and advancements in home dialysis care.

Virtual Summit Event Dates: July 16-17, 2020

If you’re interested in this timely, free summit to learn more about your kidneys and Covid-19 – and/or for any of the other topics – you can register at https://aakp.org/programs-and-events/2nd-annual-global-summit-global-kidney-innovations-expanding-patient-choices-outcomes/.

Until next week,

Keep living your life!

How Sweet It Isn’t

Hello again. Last week when I was writing about Bipolar Disorder and Chronic Kidney Disease, I mentioned nephrogenic diabetes insipidus. During the week I realized how little I know about that.

Let’s start by going back and reviewing what I wrote last week:

“What is nephrogenic diabetes insipidus?
The most common problem from taking lithium is a form of diabetes due to kidney damage called nephrogenic diabetes insipidus. This type of diabetes is different than diabetes mellitus caused by high blood sugar. In nephrogenic diabetes insipidus, the kidneys cannot respond to anti-diuretic hormone (ADH), a chemical messenger that controls fluid balance. This results in greater than normal urine out-put and excessive thirst. It can be hard to treat nephrogenic diabetes insipidus.”

Frankly, that’s not enough information for me, although it’s pretty clear. Former English teacher here. Let’s take a look at the words themselves. Keep in mind, this is what I learned along the years.

Nephro = kidneys

Genic = Beginning in

So we know this disease begins in the kidneys. And diabetes? According to Michigan State University at https://www.canr.msu.edu/news/how_diabetes_got_its_name,

“The ancient Greek word for diabetes means, ‘passing though; a large discharge of urine.’ The meaning is associated with frequent urination, which is a symptom of diabetes.”

And finally insipidus. I found myself turning to Wikipedia at https://en.wikipedia.org/wiki/Diabetes_insipidus#:~:text=”Insipidus”%20comes%20from%20Latin%20language,or%20zest%3B%20not%20tasty for help with this.

” ‘Insipidus’ comes from Latin language insipidus (tasteless), from Latin: in- ‘not’ + sapidus ‘tasty’ from sapere ‘have a taste’ — the full meaning is ‘lacking flavor or zest; not tasty’.”

This one I didn’t quite get. Back to the above link to figure out what tasteless has to do with this disease.

“Application of this name to DI arose from the fact that diabetes insipidus does not cause glycosuria (excretion of glucose into the urine).”

Ah, so the urine is not sweet. Reminder: Diabetes can be diagnosed by the doctor tasting the urine. While this was more common in the 1600s, I have read about doctors tasting urine for diabetes more recently and even currently. If the urine is sweet, diabetes is present.

This is interesting. I’d never considered a form of diabetes that didn’t deal with blood glucose, which may also be called blood sugar, so sweet. Of course, I then began to wonder if taking lithium was the only way to develop this disease. The Mayo Clinic at https://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/symptoms-causes/syc-20351269#:~:text=Nephrogenic%20diabetes%20insipidus%20occurs%20when,or%20a%20chronic%20kidney%20disorder was quite a bit of help here:

“Nephrogenic diabetes insipidus occurs when there’s a defect in the kidney tubules — the structures in your kidneys that cause water to be excreted or reabsorbed. This defect makes your kidneys unable to properly respond to ADH.

The defect may be due to an inherited (genetic) disorder or a chronic kidney disorder. Certain drugs, such as lithium or antiviral medications such as foscarnet (Foscavir), also can cause nephrogenic diabetes insipidus.”

This is a lot of new information to understand unless we get more help. Let’s take a look at kidney tubules now. I turned to my old favorite Healthline at https://www.healthline.com/health/human-body-maps/kidney#nephrons and found the following:

“Each tubule has several parts:

  • Proximal convoluted tubule. This section absorbs water, sodium, and glucose back into the blood.
  • Loop of Henle. This section further absorbs potassium, chloride, and sodium into the blood.
  • Distal convoluted tubule. This section absorbs more sodium into the blood and takes in potassium and acid.

By the time fluid reaches the end of the tubule, it’s diluted and filled with urea. Urea is byproduct of protein metabolism that’s released in urine.”

That makes sense, but what about this ADH? What is that?  My Health Alberta Ca at https://myhealth.alberta.ca/Health/pages/conditions.aspx?hwid=hw211268 tells us:

“Antidiuretic hormone (ADH) is a chemical produced in the brain that causes the kidneys to release less water, decreasing the amount of urine produced. A high ADH level causes the body to produce less urine. A low level results in greater urine production.

Normally, the amount of ADH in the body is higher during the night. This helps prevent urination while you are sleeping. But if the levels of ADH remain low during the night, the body will produce large amounts of urine, so urination during the night is more likely.”

We know how you can develop nephrogenic diabetes insipidus, but how do you treat it once you’ve been diagnosed? WebMD at https://www.webmd.com/diabetes/guide/nephrogenic-diabetes-insipidus-symptoms-causes-and-treatments offers us the following:

“If a drug like lithium is responsible, switching medicines might improve nephrogenic diabetes insipidus.

Most adults with nephrogenic diabetes insipidus are able to keep up with fluid losses by drinking water. For some people, though, the symptoms of near-constant thirst and urination can become intolerable. Some treatments can reduce the symptoms of nephrogenic diabetes insipidus, at least somewhat:

All adults and children with nephrogenic diabetes insipidus should take frequent bathroom breaks. This helps to avoid over-distending the bladder, which can cause long-term problems, though rarely.

The most important treatment for nephrogenic diabetes insipidus is to ensure constant access to lots of water. Not keeping up with fluid losses can lead to dehydration or electrolyte imbalances, which can sometimes be severe. Seek medical help if symptoms don’t improve after rehydrating, eating fresh fruit, and taking a multivitamin.”

Now, the biggie…. Is this rare disease curable? Unfortunately it isn’t, although,

“For individuals with acquired NDI treating the underlying cause (e.g., correcting metabolic imbalances or discontinuing drug use) can reverse the kidneys resistance to vasopressin. [Gail here again: Vasopressin is another name for ADH as far as I can tell.] However, this reversal may take weeks. In some cases caused by the use of drugs such as lithium, it may take years for the kidneys to respond to vasopressin again or it can become irreversible.”

Thank you to National Organization for Rare Diseases (NORD) at https://rarediseases.org/rare-diseases/nephrogenic-diabetes-insipidus/ for the above information.

I feel like I’ve been down the rabbit hole with Alice with all this new information about a rare disease that your already existing kidney disease may cause. Hopefully, you won’t be one of its victims.

Until next week,

Keep living your life!

Bipolar Disorder and Chronic Kidney Disease

It turns out I know more people with bipolar disorder than I’d thought. Of course, that led me to wonder again what, if anything, this might have to do with CKD. That’s just the way my mind works. Everything – and I do mean everything – leads back to CKD for me. So, as usual, I started asking them questions and poking around on the internet.

It seems that most of them are taking lithium to help control the bipolar disorder. Okay, I’ll bite: what is lithium? Drugs.com at https://www.drugs.com/lithium.html has quite a lot to say about this drug, but I’ll start with the basic definition:

Lithium affects the flow of sodium through nerve and muscle cells in the body. Sodium affects excitation or mania.

Lithium a mood stabilizer that is a used to treat or control the manic episodes of bipolar disorder (manic depression). Manic symptoms include hyperactivity, rushed speech, poor judgment, reduced need for sleep, aggression, and anger.

Lithium also helps to prevent or lessen the intensity of manic episodes.”

Notice sodium is mentioned. Keep that in mind while we backtrack for a definition of bipolar disorder. It seems I jumped right in without giving you some of the necessary background information. I’ll rectify that right now.

The National Institute of Mental Health at https://www.nimh.nih.gov/health/topics/bipolar-disorder/index.shtml tells us:

“Bipolar disorder (formerly called manic-depressive illness or manic depression) is a mental disorder that causes unusual shifts in mood, energy, activity levels, concentration, and the ability to carry out day-to-day tasks.

There are three types of bipolar disorder. All three types involve clear changes in mood, energy, and activity levels. These moods range from periods of extremely ‘up,’ elated, irritable, or energized behavior (known as manic episodes) to very ‘down,’ sad, indifferent, or hopeless periods (known as depressive episodes). Less severe manic periods are known as hypomanic episodes.

  • Bipolar I Disorder— defined by manic episodes that last at least 7 days, or by manic symptoms that are so severe that the person needs immediate hospital care. Usually, depressive episodes occur as well, typically lasting at least 2 weeks. Episodes of depression with mixed features (having depressive symptoms and manic symptoms at the same time) are also possible.
  • Bipolar II Disorder— defined by a pattern of depressive episodes and hypomanic episodes, but not the full-blown manic episodes that are typical of Bipolar I Disorder.
  • Cyclothymic Disorder (also called Cyclothymia)— defined by periods of hypomanic symptoms as well as periods of depressive symptoms lasting for at least 2 years (1 year in children and adolescents). However, the symptoms do not meet the diagnostic requirements for a hypomanic episode and a depressive episode.

Sometimes a person might experience symptoms of bipolar disorder that do not match the three categories listed above, which is referred to as ‘other specified and unspecified bipolar and related disorders’ .”

In the July 3rd, 2017, blog, I wrote about those who already have CKD and then develop bipolar disorder.

“Kidney.org at https://www.kidney.org/atoz/content/lithium has me downright frightened for my friend…

“How does lithium cause kidney damage?
Lithium may cause problems with kidney health. Kidney damage due to lithium may include acute (sudden) or chronic (long-term) kidney disease and kidney cysts. The amount of kidney damage depends on how long you have been taking lithium. It is possible to reverse kidney damage caused by lithium early in treatment, but the damage may become permanent over time.

What is nephrogenic diabetes insipidus?
The most common problem from taking lithium is a form of diabetes due to kidney damage called nephrogenic diabetes insipidus. This type of diabetes is different than diabetes mellitus caused by high blood sugar. In nephrogenic diabetes insipidus, the kidneys cannot respond to anti-diuretic hormone (ADH), a chemical messenger that controls fluid balance. This results in greater than normal urine out-put and excessive thirst. It can be hard to treat nephrogenic diabetes insipidus.”

As we can see, this is not the first time I’ve written about a dual diagnose of these two diseases – one mental, one physical – and how they affect each other. One of the interesting facts I found is that you need to tell your doctor if you have kidney disease when he prescribes lithium. None of my friends has CKD yet, although one is under surveillance (if that’s the proper word) since she’s having some decline in her eGFR.

Remember I asked you to keep that sodium reference in mind? One problem with lithium is that it requires you to include sodium in your diet. As a CKD patient, you’re asked to limit your sodium intake. You can’t do both at once. This is from WebMD at https://www.webmd.com/bipolar-disorder/guide/bipolar-disorder-lithium#2:

“Tell your doctor about history of cancerheart diseasekidney diseaseepilepsy, and allergies. Make sure your doctor knows about all other drugs you are taking. Avoid products that are low in sodium (salt) since a low sodium diet can lead to excessively high lithium levels.

So what can you do to protect your kidneys if you must take lithium for your mental health? This is what Psychiatric Times at https://www.psychiatrictimes.com/view/6-ways-protect-kidneys-while-prescribing-lithium has to say about the subject:

Tip 1. Avoid toxicity

The link between lithium and renal dysfunction may be explained by exposure to toxic lithium levels. Toxic levels kill renal cells, and that damage builds up every time the level rises above the toxic line….

Tip 2. Keep the level low

Keeping the lithium level as low as possible can prevent renal impairment. The ideal level needs to be personalized and tends to fall with age….

Tip 3. Dose lithium once a day

Dosing lithium once in the evening reduces the risk of renal problems….

If high serum levels are needed to treat active mania, dosing twice a day may be necessary to avoid toxic peaks. The line of toxicity is different for each patient because it’s defined by symptoms.…

Tip 4. Drinking and urinating too much

Polyuria and polydipsia are common adverse effects of lithium (30% to 80%), and they are not always benign. When severe, they may indicate nephrogenic diabetes insipidus (NDI), which means that changes in the renal tubules are impeding the kidneys ability to concentrate the urine. Those changes raise the risk of future renal impairments.

Besides stopping lithium, the main treatment for NDI is amiloride, a potassium sparing diuretic (5 mg po qd). Amiloride may prevent further renal problems by reducing fibrotic changes in the kidneys…. This medication is best managed through consultation with the medical team because it carries a risk of hyperkalemia, particularly in patients with renal insufficiency or diabetes.

Tip 5. Consider N-Acetylcysteine

N-Acetylcysteine (NAC) is an antioxidant that can protect and even reverse renal toxicity, including toxicity from lithium…. NAC is part of a healthy diet, and the capsule form is safe, well-tolerated (the main risk is constipation), and inexpensive. Sounds like a winner, but there is one catch. The renal studies…were all done in animals.

However, there is another reason to use NAC in bipolar disorder. This supplement is effective for bipolar depression in some, but not all, studies… and those benefits are more pronounced in the medically ill….

The dose in bipolar disorder (2000 mg/day) is about twice the amount that was used for renal protection (10 mg/kg)….

Tip 6. Measure

Renal function should be monitored every 3 to 6 months on lithium. Older patients benefit from more frequent monitoring, as do those with a history of toxicity, high serum levels, or drug interactions. Creatinine is usually sufficient, but a more accurate measure of renal function is the estimated glomerular filtration rate (eGFR)….

Laboratory changes that should prompt a nephrology consult include:

  • eGFR < 30 ml/min/1.73m2
  • Creatinine ≥ 1.5 mg/dL
  • A decline of eGFR by more than 4 ml/min/1.73m… per year….”

There’s more, much more, on this site if you’re interested.

Until next week,

Keep living your life!

 

A Different Kind of App  

Periodically for the last decade, I’ve written about apps that could help us manage our Chronic Kidney Disease. They would be those with electrolyte counters, portion counters, GFR calculators, and even calorie counters or exercise counters. They were helpful. Some still exist; some have gone by the wayside.

In recent years, I’ve been vocal about the necessity for CKD patients to understand what our disease is, how it came to be, and what we might do about it. This is different from wanting people to be aware of CKD. My contention is that the educated patient is the one most able to help him or herself.

Responsum for CKD does just that, but I’ll let them explain their app themselves. This is from their April 28th blog at https://responsumhealth.com/great-news-for-the-ckd-community/.

“I have great news to share with Responsum Health’s extended family of supporters and everyone around the world whose lives are affected by kidney disease. Responsum Health, with support from Otsuka Pharmaceutical, is launching a new platform and app designed specifically for people with kidney disease, including chronic kidney disease (CKD)—a condition that affects 37 million Americans.

Responsum for CKD represents our company’s second disease-specific platform—the first being Responsum for PF—and includes some amazing new features. These include a translation function into seven languages and a dynamic social wall called Community Chat, which automatically suggests articles and resources based upon each comment or entry. Just like with pulmonary fibrosis, Responsum for CKD will be available as a free web-based platform and a mobile app for iOS and Android.

We’ve recruited an all-star Content Advisory Council made up of some of the top specialists in CKD to serve as our content validators. Instead of partnering with a specific patient advocacy group to vet our content, we chose this approach to ensure that the platform is free of commercial bias. We will roll out the names of our esteemed council alongside the app launch.

To the CKD community, Responsum Health is on the way! We can’t wait to serve you, join you, learn from you, and listen to you.

Let’s get started!

Andy Rosenberg
Founder and CEO, Responsum Health

Perhaps we could use a bit more information. Let’s try their May 5th press release at https://responsumhealth.com/press-and-media/responsum-health-launches-innovative-kidney-disease-information-platform/.

“Responsum Health Launches Innovative Kidney Disease Information Platform
New technology supports patients, families, caregivers, and healthcare professionals

​[WASHINGTON, D.C., May 28 2020] — Today, Responsum Health (Responsum), an innovative developer of personalized patient apps and chronic disease knowledge communities, with support from Otsuka Pharmaceutical, a global healthcare company, announced the launch of an online connection and knowledge platform for patients with kidney disease, such as chronic kidney disease (CKD), a condition that affects an estimated 37 million Americans. The platform, called Responsum for CKD, can be accessed for free via web browser or mobile app.

Designed to meet the needs of patients, families, caregivers, and healthcare professionals, Responsum for CKD offers a number of informational and community-oriented features. At its core, Responsum replaces unreliable web aggregators and social sites by providing patients and caregivers with a customized Newsfeed that has easy-to-read summaries of important kidney health news items. All of the information found on Responsum’s platforms is written by professional health writers and vetted by a team of researchers under the guidance of an advisory council, which is made up of leading kidney health experts.

Other features include a moderated social wall to serve as a community chat room and the Patient One-Sheet, which allows patients to easily collect, download, print, and share their key medical information. Patients will also have access to a robust collection of trusted patient support links.

“We are grateful that Otsuka is willing to support our mission to educate, support, and empower patients with chronic conditions through our unique approach to providing patients with the information they need to drive better outcomes,” said Andrew Rosenberg, founder of Responsum Health. “By working with recognized leaders from the patient advocacy community, we have created a trusted online platform that fills a vital information gap—while simultaneously creating an authentic, welcoming online community for people with kidney disease.”

About Responsum Health

Responsum Health’s mission is to build and support online knowledge communities for chronic disease patients. The company offers a free, revolutionary patient engagement platform that monitors, searches, and curates the Internet to generate a personalized news feed of article summaries, which are vetted by Responsum’s patient group partners. Responsum wraps the news feed into a comprehensive platform that enables patients to comment on and rate the articles, as well as share them with their professional care team and loved ones. Responsum also enables patients to better organize their health information, find local patient support groups and services, and support one another through a moderated, disease-specific social wall.”

The one thing that has been missing from other CKD apps is the education. I write to help people become aware of CKD and maybe understand a little bit of what affects you as a CKD patient. Responsum has articles in real time, so to speak. What I mean by that is if you’re interested in potassium and ask a question in the community about it, you also have articles attached that will explain more about your topic: no searching, no delay, just click on the upper right hand corner. How marvelous.

I think I’ve mentioned that I’ve been involved in what we used to call think tanks about what CKD patients need. My answer has always been education… and what could be better than immediate education? The one sheet with your medical information is also a boon, but not specific to only this app.

But the community with instant articles about your topic? Priceless. I would say that it’s free is also priceless, but that’s a little bit obvious. Do I recommend this app? Yes. Do I use this app? Yes… and if asked my opinion, I would say you should use it, too. The key to our kidney health just may be self-education.

Until next week,

Keep living your life!

Echo… Echo… Echo…

Remember that golden time I’ve mentioned before? The time when I problem solve and write in my head just as I’m waking up? Well, today the word was echo at that time. Echo? As in echo chamber? Echo Canyon? No, doesn’t feel right. Got it! Echocardiogram.

The English teacher in me is already delighted. Why? I know what most of the word means through my college study of Greek and Latin roots. Card means heart, io is simply a connective, and gram means write. What about echo you ask? I think we all know what that means in common usage, but in conjunction with cardiogram? Yep, time for some help.

The Merriam-Webster Dictionary, still my favorite, at https://www.merriam-webster.com/dictionary/ echocardiography tells us an echocardiogram is,

“the use of ultrasound to examine the structure and functioning of the heart for abnormalities and disease”

Let’s put in a little reminder of what an ultrasound is here. This is from MedicineNet at https://www.medicinenet.com/script/main/art.asp?articlekey=5897:

“A test in which high-frequency sound waves (ultrasound) are bounced off tissues and the echoes are converted into a picture (sonogram).”

Oh, like the picture of my grandson growing in his mom’s womb. Great, now what does this have to do with Chronic Kidney Disease? I just had an echocardiogram because my oncologist was concerned about the great distance between my diastolic (lower) and systolic (upper) numbers on my blood pressure readings. It was fine, but it did get me to thinking about what CKD and the heart have in common.

Here’s a reminder from Healthline at https://www.healthline.com/health/diastole-vs-systole#:~:text=Your%20systolic%20blood%20pressure%20is,bottom%20number%20on%20your%20reading of what the two numbers mean:

“Your systolic blood pressure is the top number on your reading. It measures the force of blood against your artery walls while your ventricles — the lower two chambers of your heart — squeeze, pushing blood out to the rest of your body.

Your diastolic blood pressure is the bottom number on your reading. It measures the force of blood against your artery walls as your heart relaxes and the ventricles are allowed to refill with blood. Diastole — this period of time when your heart relaxes between beats — is also the time that your coronary artery is able to supply blood to your heart.”

Got it. This next quote is a little medicalese, but basically it’s saying there are specific difficulties if you have both CKD and high blood pressure. It’s from Kidney International at https://www.kidney-international.org/article/S0085-2538(19)30276-5/fulltext :

“In CKD and ESKD, risk factors for HF include long-standing hypertension with often worsened blood pressure (BP) control as CKD worsens, salt and water retention causing excessive preload, and cardiomyopathic factors including left ventricular (LV) hypertrophy and fibrosis. In addition, there are CKD- and ESKD-specific factors that affect afterload (increased arterial stiffness and high output shunting through arteriovenous fistulae or grafts) as well as load-independent factors (neurohormonal activation, impaired iron utilization, anemia, demand ischemia, profibrotic factors [e.g., fibroblast growth factor 23 {FGF-23}], inflammation, etc.)…. Arteriovenous fistulae or grafts have been reported to worsen right ventricular hypertrophy, increase pulmonary pressures, associate with significant right ventricular dilatation, and reduce right ventricular function, which are closely linked to survival….”

An echocardiogram can show in real time if all the ventricles of your heart are working correctly as far as pumping blood and and/or leaking when your heart should be at rest.

Well, why get an echocardiogram if you already know you have CKD and high blood pressure? Here’s WebMD at https://www.webmd.com/heart-disease/guide/diagnosing-echocardiogram#4’s response.  You can find much more information there, too, as is true of all the sites mentioned.

“An echocardiogram can help your doctor diagnose several kinds of heart problems, including:

  • An enlarged heart or thick ventricles (the lower chambers)
  • Weakened heart muscles
  • Problems with your heart valves
  • Heart defects that you’ve had since birth
  • Blood clots or tumors”

Mayo Clinic at https://www.mayoclinic.org/tests-procedures/echocardiogram/about/pac-20393856 offers an easily understandable explanation of the actual process. There are many types of echocardiograms, but this is the most usual.

Transthoracic echocardiogram

In this standard type of echocardiogram:

  • A technician (sonographer) spreads gel on a device (transducer).
  • The sonographer presses the transducer firmly against your skin, aiming an ultrasound beam through your chest to your heart.
  • The transducer records the sound wave echoes from your heart.
  • A computer converts the echoes into moving images on a monitor.”

This is yet another reminder of why we need to have both the heart and kidneys functioning well. This one is from Heart.org at https://www.heart.org/en/health-topics/high-blood-pressure/health-threats-from-high-blood-pressure/how-high-blood-pressure-can-lead-to-kidney-damage-or-failure#:~:text=The%20:

  • Damaged kidney arteries do not filter blood well. Kidneys have small, finger-like nephrons that filter your blood. Each nephron receives its blood supply through tiny hair-like capillaries, the smallest of all blood vessels. When the arteries become damaged, the nephrons do not receive the essential oxygen and nutrients — and the kidneys lose their ability to filter blood and regulate the fluid, hormones, acids and salts in the body.
  • Damaged kidneys fail to regulate blood pressure. Healthy kidneys produce a hormone called aldosterone to help the body regulate blood pressure. Kidney damage and uncontrolled high blood pressure each contribute to a negative spiral. As more arteries become blocked and stop functioning, the kidneys eventually fail.”

The American Journal of Kidney Disease at https://www.ajkd.org/article/S0272-6386(18)30598-5/fulltext gives us these final words on why an echocardiogram could be necessary for certain CKD patients:

“Abnormal cardiac structure and function are common in chronic kidney disease (CKD) and end-stage renal disease (ESRD) and linked with mortality and heart failure.”

Topic change: We tried Flavis’s high protein spaghetti and found it just as light and delightful as their penne. This, I can endorse.

Oh, before I forget. I like to read… a lot. One of the books I read recently was Ray Flynt’s Transplanted Death. I don’t want to tell you too much about it, except that it is a well-written murder mystery with a good story that revolves around transplant recipients, two of them kidney recipients. I am recommending this book.

Until next week,

Keep living your life!