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! 

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! 

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!

Is it Blood Sugar or the Pancreas?

We all know diabetes raises your risk of developing Chronic Kidney Disease. But why? What’s the mechanism behind the fact? As far as I’m concerned, it’s time to find out.

Let’s start with diabetes. The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH), which in turn is part of The U.S. Department of Health and Human Services at https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes offers this explanation.

“Diabetes is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body doesn’t make enough—or any—insulin or doesn’t use insulin well. Glucose then stays in your blood and doesn’t reach your cells.

Over time, having too much glucose in your blood can cause health problems. Although diabetes has no cure, you can take steps to manage your diabetes and stay healthy.

Sometimes people call diabetes ‘a touch of sugar’ or ‘borderline diabetes.’”

Having just had a tumor removed from my pancreas, I’m well aware that it produces insulin as well as digestive enzymes. Without a pancreas to produce insulin, you would need insulin injections several times a day.

I got what diabetes is, but how it causes CKD was still not clear.

Well, not until I read the following from The American Diabetes Association at https://www.diabetes.org/diabetes/complications/kidney-disease-nephropathy.

“When our bodies digest the protein we eat, the process creates waste products. In the kidneys, millions of tiny blood vessels (capillaries) with even tinier holes in them act as filters. As blood flows through the blood vessels, small molecules such as waste products squeeze through the holes. These waste products become part of the urine. Useful substances, such as protein and red blood cells, are too big to pass through the holes in the filter and stay in the blood.

Diabetes can damage this system. High levels of blood sugar make the kidneys filter too much blood. All this extra work is hard on the filters. After many years, they start to leak and useful protein is lost in the urine. Having small amounts of protein in the urine is called microalbuminuria.

When kidney disease is diagnosed early, during microalbuminuria, several treatments may keep kidney disease from getting worse. Having larger amounts of protein in the urine is called macroalbuminuria. When kidney disease is caught later during macroalbuminuria, end-stage renal disease, or ESRD, usually follows.

In time, the stress of overwork causes the kidneys to lose their filtering ability. Waste products then start to build up in the blood. Finally, the kidneys fail. This failure, ESRD, is very serious. A person with ESRD needs to have a kidney transplant or to have the blood filtered by machine (dialysis).”

Hmmm, now that we know what diabetes is and how it can cause CKD, maybe we need to look at ways to attempt to avoid diabetes.

  • Losing weight and keeping it off. Weight control is an important part of diabetes prevention. You may be able to prevent or delay diabetes by losing 5 to 10 percent of your current weight. For example, if you weigh 200 pounds, your goal would be to lose between 10 to 20 pounds. And once you lose the weight, it is important that you don’t gain it back.
  • Following a healthy eating plan. It is important to reduce the amount of calories you eat and drink each day, so you can lose weight and keep it off. To do that, your diet should include smaller portions and less fat and sugar. You should also eat a variety of foods from each food group, including plenty of whole grains, fruits, and vegetables. It’s also a good idea to limit red meat, and avoid processed meats.
  • Get regular exercise. Exercise has many health benefits, including helping you to lose weight and lower your blood sugar levels. These both lower your risk of type 2 diabetes. Try to get at least 30 minutes of physical activity 5 days a week. If you have not been active, talk with your health care professional to figure out which types of exercise are best for you. You can start slowly and work up to your goal.
  • Don’t smoke. Smoking can contribute to insulin resistance, which can lead to type 2 diabetes. If you already smoke, try to quit.
  • Talk to your health care provider to see whether there is anything else you can do to delay or to prevent type 2 diabetes. If you are at high risk, your provider may suggest that you take one of a few types of diabetes medicines.”

This is a list from NIH: National Institute of Diabetes and Digestive and Kidney Diseases posted on MedLinePlus at https://medlineplus.gov/howtopreventdiabetes.html. Notice it’s mentioned that this is for type 2 diabetes.

There are 11 different kinds of diabetes. Types 1 and 2 are the most common. WebMD at https://www.webmd.com/diabetes/guide/types-of-diabetes-mellitus#1 explains what type 1 and 2 are.

Type 1 diabetes is an autoimmune condition. It’s caused by the body attacking its own pancreas with antibodies. In people with type 1 diabetes, the damaged pancreas doesn’t make insulin…. With Type 2 diabetes, the pancreas usually produces some insulin. But either the amount produced is not enough for the body’s needs, or the body’s cells are resistant to it. Insulin resistance, or lack of sensitivity to insulin, happens primarily in fat, liver, and muscle cells.”

This is all starting to make sense.

Until next week,

Keep living your life!

Diabetic Neuropathy or Not: I WILL Dance Again

I come from a family of dancers. My parents and their siblings were all light on their feet and danced from the time they were teens right up until just before their deaths. It was a delight to watch them. The tradition continued with me… and my youngest who actually taught blues dancing for several years.

Ah, but then my neuropathy appeared. This was years before the diabetes diagnosis. Hmmm, there’s still a question as to whether or not the diabetes was caused by the pancreatic cancer. After all, the pancreas does produce insulin.

I just reread the above two paragraphs and see so much that needs some basic explanation. Let’s start with those explanations this week. How many of you know what neuropathy is? I didn’t either until I was diagnosed with it. According to my favorite dictionary since college a million years ago, The Merriam-Webster Dictionary at https://www.merriam-webster.com/dictionary/neuropathy defines neuropathy as:

“damage, disease, or dysfunction of one or more nerves especially of the peripheral nervous system that is typically marked by burning or shooting pain, numbness, tingling, or muscle weakness or atrophy, is often degenerative, and is usually caused by injury, infection, disease, drugs, toxins, or vitamin deficiency “

If you clicked though on ‘peripheral nervous system’ in the dictionary definition, you know it means,

“the part of the nervous system that is outside the central nervous system and comprises the cranial nerves excepting the optic nerve, the spinal nerves, and the autonomic nervous system”

Since the neuropathy was so minor before the pancreatic cancer, I wasn’t even aware of it until my neurologist did some testing. I knew my feet were tingly sometimes, but I thought they had fallen asleep. It did sort of feel like that.

Then, I started chemotherapy in March. The tingling became so bad that I couldn’t feel my feet under me and had to rely on a cane to keep my balance. We thought it was the chemo drugs causing the neuropathy. Uh-oh, that was just about when my hands became affected, too, and my A1C (Remember that one? It’s the blood test for the average of your blood glucose over a three month period.) rose all the way to 7.1.

Healthline at https://www.healthline.com/health/type-2-diabetes/ac1-test#understanding-the-results tells us,

“Someone without diabetes will have about 5 percent of their hemoglobin glycated [Gail here: that means glucose bonded to hemoglobin]. A normal A1C level is 5.6 percent or below, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

A level of 5.7 to 6.4 percent indicates prediabetes. People with diabetes have an A1C level of 6.5 percent or above.”

Mind you, during chemotherapy I’d been ordered to eat whatever I could. Getting in the calories would cut down on the expected weight loss. In all honesty, I’m the only person I know what gained weight while on chemotherapy.

Now, what is this about the pancreas producing insulin? Might as well get a definition of insulin while we’re at it. MedicineNet at https://www.medicinenet.com/script/main/art.asp?articlekey=3989 offered the simplest explanation:

“A natural hormone made by the pancreas that controls the level of the sugar glucose in the blood. Insulin permits cells to use glucose for energy. Cells cannot utilize glucose without insulin.”

That would explain why my energy is practically nil, but it also seems to indicate that I won’t be able to do anything about it until after the surgery to remove the tumor. Although, when I start radiation next week, I may be able to go back to the diabetic diet. By the way, after following the Chronic Kidney Disease diet for 11 years, none of the new – off the CKD diet – foods I tried are appealing to me.

But I digress. So, what now? I need to dance; it’s part of who I am. My oncologist referred me to Occupational Therapy. Now I have exercises and tactile surfaces to explore that may be helpful. But what about those who are not going through chemotherapy, but do have diabetic neuropathy? Remember diabetes is the number cause of CKD.

Oh, my goodness. It looks like there are as many ways to treat neuropathy as there are different kinds of neuropathy. I hadn’t expected that. EverydayHealth at https://www.everydayhealth.com/neuropathy/guide/treatment/ gives us an idea of just how complicated choosing the proper treatment for your neuropathy can be:

What Are the Main Ways That Neuropathy Is Treated?

Treating neuropathy in general focuses first on identifying and then addressing the underlying condition to help prevent further damage and give nerves the time they need to heal to the extent that they can.

“The treatment for the neuropathy is to reverse whatever it is that is causing the neuropathy,” says Clifford Segil, DO, a neurologist at Providence Saint John’s Health Center in Santa Monica, California. “We try to reverse the insult to the nerves first and then do symptomatic control.”

For people with diabetic neuropathy, the first step physicians take is getting the person’s blood glucose level under control, says Matthew Villani, DPM, a podiatrist at Central Florida Regional Hospital in Sanford, Florida.

This treatment approach aims to remove the “insult” created by the excess sugar to peripheral nerves throughout the body — but especially the extremities, Dr. Segil explains.

Here are some other ways diabetic neuropathy may be treated:

  • Numbness or complete loss of sensation can lead to complications such as ulcers, sores, and limb amputations. It is addressed by monitoring the affected areas — often the feet — for injuries and addressing wounds before they become more serious, as well as prescribing protective footwear and braces.
  • Orthostatic hypotension (a drop in blood pressure upon standing up), which is an autonomic symptom, can be treated with increased sodium intake, a vasopressor such as ProAmatine (midodrine) to constrict blood vessels, a synthetic mineralocorticoid such as fludrocortisone to help maintain the balance of salt in the body, or a cholinesterase inhibitor such as pyridostigmine, which affects neurotransmitters.
  • Gastroparesis, a delayed emptying of the stomach, is another autonomic symptom, which can be treated with medication to control nausea and vomiting, such as Reglan (metoclopramide), Ery-Tab (erythromycin), antiemetics, and antidepressants, as well as pain medication for abdominal discomfort.
  • Motor neuropathy symptoms can include weakness and muscle wasting, particularly in the lower extremities, as well as deformities of the feet and loss of the Achilles’ heel tendon reflex. Treatments can include physical therapy to regain strength, as well as braces and orthotics.

I’ve got to think about this. Any questions? Well, then,

Until next week,

Keep living your life!

Chemo and My Kidneys

 As most of you know, I am extremely protective of my kidneys. When I was first diagnosed with Chronic Kidney Disease 11 years ago, my eGFR was only 39. Here’s a quick reminder of what the eGFR is from my first CKD book, What Is It and How Did I Get It? Early Stage Chronic Kidney Disease:

“GFR: Glomerular filtration rate [if there is a lower case ‘e’ before the term, it means estimated glomerular filtration rate] which determines both the stage of kidney disease and how well the kidneys are functioning.”

39. That’s stage 3B, the lower part of stage 3B. During the intervening 11 years, I’ve been able to raise it to 50 (and sometimes higher for short periods) via vigorously following the renal diet, exercising, avoiding stress as much as possible, maintaining adequate sleep, and paying strict attention to the medications prescribed for me. While the medications were the ones I had been taking for high blood pressure prior to being diagnosed with CKD, they worked in my favor.

This excerpt from The National Center for Biotechnology Information (NCBI) part of the United States National Library of Medicine (NLM), a branch of the National Institutes of Health (NIH) at https://www.ncbi.nlm.nih.gov/books/NBK492989/ will explain why:

“The decision of whether to reduce blood pressure levels in someone who has chronic kidney disease will depend on

  • how high their blood pressure is (when untreated),
  • whether they have diabetes, and
  • how much protein is in their urine (albumin level).

A person with normal blood pressure who doesn’t have diabetes and hardly has any albumin in their urine will be able to get by without using any blood-pressure-lowering medication. But people who have high blood pressure, diabetes or high levels of albumin in their urine are advised to have treatment with ACE inhibitors (angiotensin-converting enzyme inhibitors) or sartans (angiotensin receptor blockers). In people who have diabetes, blood-sugar-lowering medication is also important.”

When I was first diagnosed with pancreatic cancer early last month, it changed my medical priorities. With my nephrologist’s blessing, my primary focus was the cancer… not my kidneys. It took constant reminders to myself not to be so quick to say no to anything that I thought would harm my kidneys. In other words, to those things I’d been saying no to for the last 11 years.

For example, once diagnosed with CKD, I ate very little protein keeping to my five ounce daily limitation. Not anymore. Protein is needed to avoid muscle wasting during chemotherapy with a minimum requirement of eight ounces a day. I even tried roast beef and other red meats. After 11 years, they no longer agreed with me so I eat ground turkey, chicken, cheese, and am considering soy.

Another change: I preferred not to eat carbohydrates, but was warned not to lose weight if I could help it. All of a sudden I’m eating Goldfish, bread, and pasta. I can’t say that I’m enjoying them, but I am keeping my weight loss to a minimum. Other limitations like those on potassium and phosphorous have also gone by the wayside. I’ve eaten every childhood favorite, foods that I’ve avoided for the last 11 years, and anything that might look tempting in the last month, but none of them really taste that good. I like the foods on the renal diet now.

Oh, the only thing I have not increased is salt. My daughter takes me to my chemotherapy sessions. There’s a Jewish style restaurant across the street and we showed up early one day. I wanted to try a toasted bagel with butter, the way I ate it before CKD. The damned thing was salty! I hadn’t expected that.

Back to chemo and my kidneys. I admit it. I was nervous. What was this combination of poisons going to do to my kidneys? If it was so caustic that I had to have a port in place so that it wouldn’t be injected directly into my veins for fear of obliterating them, what about my kidneys?

I anxiously awaited my first Comprehensive Blood Panel, the blood test that includes your GFR. Oh, oh, oh! My kidney function had risen to 55 and my creatinine had lowered to 1.0. Let me explain just how good this was.

A GFR of 55 is the higher part of stage 3A. 60 is where stage 2 of CKD begins. My kidneys were functioning better on chemo. And the creatinine? Let’s get a quick definition of that first. According to The National Institute of Diabetes and Digestive and Kidney Diseases at https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd/tests-diagnosis:

“Creatinine. Creatinine is a waste product from the normal breakdown of muscles in your body. Your kidneys remove creatinine from your blood. Providers use the amount of creatinine in your blood to estimate your GFR. As kidney disease gets worse, the level of creatinine goes up.”

Yet, mine went down. How? I asked and it was explained that all the hydration used to clear my veins of the caustic chemotherapy had worked this magic. I had two hours of hydration before the chemo-therapy  itself, two hours afterward, and another two hours the next day. My kidneys had never been this hydrated!

But wait, there’s more. I have diabetes. The pancreas is the organ that produces insulin. Could my diabetes be from the tumor blocking the production of insulin by my pancreas? I truly don’t know, but my glucose level is within the standard range for the first time since I’ve been diagnosed with diabetes.

Would I recommend chemotherapy to raise your GFR, and lower your creatinine and your glucose level? Of course not. But I am feeling so very lucky that my kidneys are not coming to any harm during the chemotherapy necessary to save my life. I can’t begin to tell you how relieved I am.

Until next week,

Keep living your life!

Pancreas + Kidneys = ?

31 years ago, my father died of pancreatic cancer. For some reason, I remember him asking me what electrolytes were as soon as he was diagnosed. I didn’t know. I do now, but I don’t know if there’s a connection between the pancreas and the kidneys. Of course, I mean other than the fact that they are all organs in your body.

Oh, sorry, I didn’t give you the definition. This is from Healthline at https://www.healthline.com/nutrition/electrolytes  :

“’Electrolyte’ is the umbrella term for particles that carry a positive or negative electric charge ….

In nutrition, the term refers to essential minerals found in your blood, sweat and urine.

When these minerals dissolve in a fluid, they form electrolytes — positive or negative ions used in metabolic processes.

Electrolytes found in your body include:

  • Sodium
  • Potassium
  • Chloride
  • Calcium
  • Magnesium
  • Phosphate
  • Bicarbonate

These electrolytes are required for various bodily processes, including proper nerve and muscle function, maintaining acid-base balance and keeping you hydrated.”

Ummm, you have Chronic Kidney Disease. These are the electrolytes you need to keep an eye on, especially sodium, potassium, and phosphate. But why did Dad ask me about them?

I plunged right in to find the answer and immediately found a journal article… on a pay site. Not being one to pay for what can be found for free (and is 30 years old, by the way), I decided to look for as much information on the pancreas as I could find and see what we could figure out together.

Let’s start at the beginning. According to the Sol Goldman Pancreatic Cancer Research Center of Johns Hopkins Medicine – Pathology at http://pathology.jhu.edu/pc/basicoverview1.php?area=ba:

“What is the pancreas?

The pancreas is a long flattened gland located deep in the belly (abdomen). Because the pancreas isn’t seen or felt in our day to day lives, most people don’t know as much about the pancreas as they do about other parts of their bodies. The pancreas is, however, a vital part of the digestive system and a critical controller of blood sugar levels.

Where is the pancreas?

The pancreas is located deep in the abdomen. Part of the pancreas is sandwiched between the stomach and the spine. The other part is nestled in the curve of the duodenum (first part of the small intestine). To visualize the position of the pancreas, try this: touch your right thumb and right ‘pinkie’ fingers together, keeping the other three fingers together and straight. Then, place your hand in the center of your belly just below your lower ribs with your fingers pointing to your left. Your hand will be the approximate shape and at the approximate level of your pancreas.”

I tried that. It’s not as easy as it sounds.

So now we sort of know what and where it is, but what does it do? No problem, Columbia University Irving Medical Center has just the info we need at http://columbiasurgery.org/pancreas/pancreas-and-its-functions:

“Exocrine Function:

The pancreas contains exocrine glands that produce enzymes important to digestion. These enzymes include trypsin and chymotrypsin to digest proteins; amylase for the digestion of carbohydrates; and lipase to break down fats. When food enters the stomach, these pancreatic juices are released into a system of ducts that culminate in the main pancreatic duct. The pancreatic duct joins the common bile duct to form the ampulla of Vater which is located at the first portion of the small intestine, called the duodenum. The common bile duct originates in the liver and the gallbladder and produces another important digestive juice called bile. The pancreatic juices and bile that are released into the duodenum, help the body to digest fats, carbohydrates, and proteins.

Endocrine Function:

The endocrine component of the pancreas consists of islet cells (islets of Langerhans) that create and release important hormones directly into the bloodstream. Two of the main pancreatic hormones are insulin, which acts to lower blood sugar, and glucagon, which acts to raise blood sugar. Maintaining proper blood sugar levels is crucial to the functioning of key organs including the brain, liver, and kidneys.”

The kidneys? Now it’s starting to make sense. We need whatever specific electrolyte balance our lab work tells us we need to keep our kidneys working in good stead and we need a well-functioning pancreas to regulate our blood sugars. Hmmm, diabetes is one of the two leading causes of CKD. It seems the pancreas controls diabetes since it creates insulin.

What could happen if the pancreas wasn’t doing its job, I wondered.  This is from the Mayo Clinic at https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227,

“Pancreatitis [Me here: that’s an inflammation of the pancreas] can cause serious complications, including:

  • Pseudocyst. Acute pancreatitis can cause fluid and debris to collect in cystlike pockets in your pancreas. A large pseudocyst that ruptures can cause complications such as internal bleeding and infection.
  • Infection. Acute pancreatitis can make your pancreas vulnerable to bacteria and infection. Pancreatic infections are serious and require intensive treatment, such as surgery to remove the infected tissue.
  • Kidney failure. Acute pancreatitis may cause kidney failure, which can be treated with dialysis if the kidney failure is severe and persistent.
  • Breathing problems. Acute pancreatitis can cause chemical changes in your body that affect your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.
  • Diabetes. Damage to insulin-producing cells in your pancreas from chronic pancreatitis can lead to diabetes, a disease that affects the way your body uses blood sugar.
  • Malnutrition. Both acute and chronic pancreatitis can cause your pancreas to produce fewer of the enzymes that are needed to break down and process nutrients from the food you eat. This can lead to malnutrition, diarrhea and weight loss, even though you may be eating the same foods or the same amount of food.
  • Pancreatic cancer. Long-standing inflammation in your pancreas caused by chronic pancreatitis is a risk factor for developing pancreatic cancer.

Did you catch kidney failure and diabetes? I believe we now know how the kidneys and pancreas are related to each other. Ah, if only I’d known how to research 31 years ago….

Until next week,

Keep living your life!

Coming Home

I’m not a joiner. I’ve never been one. That’s why I was so surprised that I joined the American Association of Kidney Patients… and even more surprised to find myself attending this year’s conference in Tampa Bay, Florida. Readers had been suggesting I do so for years, but I’m not a joiner. Let’s change that; I wasn’t a joiner. The AAKP conference made the difference.

What’s that you ask? Of course, you need to know what they are. This is from their website at https://aakp.org/,

THE INDEPENDENT VOICE OF KIDNEY PATIENTS SINCE 1969™

The American Association of Kidney Patients is dedicated to improving the quality of life for kidney patients through education, advocacy, patient engagement and the fostering of patient communities.

Education

The American Association of Kidney Patients (AAKP) is recognized as the leader for patient-centered education – continually developing high quality, professionally written, edited and reviewed educational pieces covering every level of kidney disease.

Advocacy

For nearly 50 years, AAKP has been the patient voice – advocating for improved access to high-quality health care through regulatory and legislative reform at the federal level. The Association’s work has improved long term outcomes in both quality of health and the ability for patients and family members affected by kidney disease to lead a more productive and meaningful life.

Community

AAKP is leading the effort to bring kidney patients together to promote community, conversations and to seek out services that help maximize patients’ everyday lives.

An IRS registered, Sec. 501(C)(3) organization, AAKP is governed by a Board of Directors. The current board is comprised of dialysis patients, chronic kidney disease patients, [Me here: You did notice ‘chronic kidney disease patients,’ right?] transplant recipients, health care professionals and members of the public concerned with kidney disease. The board and membership are serviced by a staff of five employees under the direction of Diana Clynes, Interim Executive Director, at the AAKP National Office located in Tampa, Florida.”

What’s not mentioned here is that the organization was started by only six patients. I find that astounding, but I’ll let them explain their history:

Founded by Patients for Patients

King County Hospital, New York

The American Association of Kidney Patients (AAKP) has a rich history in patient advocacy and kidney disease education. AAKP started in 1969 with six dialysis patients at King County Hospital in Brooklyn, New York. They wanted to form an organization that would elevate the kidney patient voice in national health care arena, provide patients with educational resources to improve their lives and give kidney patients and their family members a sense of community. They met twice a week in the hospital ward and while hooked up to primitive dialysis machines for 12 to 18 hours at a time they brainstormed, researched and eventually formed AAKP.

The group originally called themselves NAPH (National Association of Patients on Hemodialysis, which later changed to AAKP). AAKP joined forces with other patient groups to fight for the enactment of the Medicare End-Stage Renal Disease (ESRD) Program, testifying before congressional committees, seeking public support and creating a newsletter (the forerunner of today’s AAKP RENALIFE) to keep everyone informed. This effort was crowned with success in 1972 when Congress enacted the program that continues to provide Medicare funding for dialysis and kidney transplantation.

After winning the initial and critical battle for the Medicare ESRD Program, AAKP turned its attention to other important issues — the need to establish a secure national organization to preserve the visibility and influence of patients with Congress and to develop national, educational and supportive programs.

Today & Beyond

AAKP has grown into a nationally recognized patient organization that reaches over 1 million people yearly. It remains dedicated to providing patients with the education and knowledge necessary to ensure quality of life and quality of health.”

This former non-joiner has found her association. I originally avoided the conferences because I thought they would be focused only on dialysis and transplant patients. Boy, was I ever wrong. Here are some of the outbreak (small group) sessions that dealt with other aspects of kidney disease:

Social Media (You’re right: I signed up for that one right away since I identify as a CKD awareness advocate.)

Dental Health

How Kidney Disease Impacts Family Members

Managing the Early Stage of CKD

Understanding Clinical Trials

Treatment Options

Staying Active

Veterans Administration

Caregiver’s Corner

Living Well with Kidney Disease

Avoid Infections

Of course, there were many outbreak sessions for dialysis and transplant patients as well. And there were two opportunities to lunch with experts. That’s where I tentatively learned about governmental aspects of our disease. There were opportunities to learn about nutrition, medications, working, and coping. I’ve just mentioned a few of the 50 different topics discussed.

The general sessions, the ones everyone attended, informed us of what the government’s national policy had to do with kidney disease, legislation, nutrition, patient centered care, and innovation in care (Keep an eye out for Third Kidney, Inc.’s August guest blog.).

I have not covered even half of what was offered during the conference. Did I mention renal friendly food was available and you could dialyze near the hotel if need be? The exhibitors went beyond friendly and explaining their products to being interested in who you were and why you were there. This was the most welcoming conference I’d been to in decades.

AAKP President Paul Conway summed up my feelings about the conference when he was interviewed by The Tampa Bay Times on the last day of the conference,

“This meeting is a way for us to bring patients together and educate them on trends that could affect their own health.”

I met so many others who have kidney disease and so many others who advocate for different types of kidney disease and patients’ rights. I was educated about so many areas, especially those I previously had known nothing about, for example, legislation. It was like coming home. Would I attend again? You bet’cha. Would I urge you to attend? At the risk of being redundant, you bet’cha.

I was so excited about AAKP that I almost didn’t leave myself enough space to tell you about yet another freebie. The Book of Blogs: Moderate Chronic Kidney Disease, Part 1 is no longer in print since it has been divided into SlowItDownCKD 2011 and SlowItDownCKD 2012. But I still have a desk copy. Let me know if you’d like it. My only restriction is that you have not received a free book from me before.

Until next week,

Keep living your life!

Eating Makes Me Hungry

I couldn’t figure it out. I had my renal diet down pat (That only took ten years, she thought snidely.) When the foods I’m sensitive to had to be removed from that diet, I worked the new-reduced-possibilities-for-food-choices diet out pretty quickly, too. But then I noticed that I was hungry pretty much only after I ate.

I’d prefer to eat only if I’m hungry, but some of my medications require food first. Okay, so I knew I had to eat at least twice a day and graze several times during the day to keep my blood glucose level. I thought I took care of that by eating a small breakfast, lunch as my main meal when I got hungry, and a much smaller, almost snack type meal for dinner.

So why did eating make me hungry? Was I not taking enough food in? Nope. I counted calories to check and was not much under my allotted 1,200 per day. So what was it?

Women’s Health at https://www.womenshealthmag.com/food/g19920742/foods-that-make-you-hungrier/ named the following seven foods that make you hungrier:

  1. Whole wheat bread
  2. Fruit juices
  3. Egg whites
  4. Green smoothies
  5. Non-fact dairy
  6. Pickles
  7. Whole wheat crackers

Hmmm, between the renal diet and my food sensitivities I don’t eat any of these. Wait, I do eat whole eggs which contain egg whites, but I think Dr. Caspero meant only the whites for the purposes of this list.

Of course, I wanted to know why these foods make you hungrier. This quote is from the same article.

“For the most part, fat, fiber, and protein help with satiation,” says Alex Caspero, R.D. “So foods without those components will likely leave you searching for your next meal in no time.”

Reminder: R.D. means registered dietician.

I don’t eat whole wheat anything because I have sensitivity to it, but doesn’t it have fiber? That’s a yes and no answer. It does have fiber, but is more processed than regular flour which means less fiber. Fiber helps to fill you up. Side bar here:  Did you know that flour of any kind has wheat in it since it’s made from one or more of the three parts of the grain? That’s mean no bread for me.

Nope, Dr. Caspero didn’t answer my question as fully as I wanted it to be answered. Back to the drawing board, boys and girls.

Wait a minute. This from the BBC at http://www.bbc.co.uk/guides/zt22mp3 looks like it’s getting close to answering my question.

“Different types of food we eat affect the brain in various ways. For example, fatty foods trick the brain into believing that you have eaten fewer calories than you actually have, causing you to overeat. This is because fatty foods such as butter and fried foods contain a lot of densely packed energy.

However, other foods give a lasting sense of fullness. Fibre triggers the release of gut hormones that make you feel full. A low fibre diet though, with little or no wholemeal produce or fruit and vegetables, may leave you open to feelings of hunger.

Foods with a low GI (glycaemic index) such as nuts, vegetables and beans release energy more slowly than high GI food such as white bread and sugar. Eating more low GI foods will suppress your hunger by increasing levels of gut hormones that help you feel fuller for longer.”

Foods with a low GI, huh? This brings me back to the lessons from the Diabetes Nutritionist my family doctor sent me to when she discovered I was (and still am four years later) pre-diabetic. Okay, I can take a hint. What are some of these low GI foods?

The American Diabetes Association at http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/understanding-carbohydrates/glycemic-index-and-diabetes.html  was able to help us out here:

“Low GI Foods (55 or less)

  • 100% stone-ground whole wheat or pumpernickel bread
  • Oatmeal (rolled or steel-cut), oat bran, muesli
  • Pasta, converted rice, barley, bulgar
  • Sweet potato, corn, yam, lima/butter beans, peas, legumes and lentils
  • Most fruits, non-starchy vegetables and carrots

Medium GI (56-69)

  • Whole wheat, rye and pita bread
  • Quick oats
  • Brown, wild or basmati rice, couscous

High GI (70 or more)

  • White bread or bagel
  • Corn flakes, puffed rice, bran flakes, instant oatmeal
  • Shortgrain white rice, rice pasta, macaroni and cheese from mix
  • Russet potato, pumpkin
  • Pretzels, rice cakes, popcorn, saltine crackers
  • melons and pineapple”

According the renal diet I follow, the Northern Arizona Council on Renal Nutrition Diet, I could eat all of these foods. According to my food sensitivities, I could only eat oatmeal, some fruits, and vegetables. Maybe that’s why eating makes me hungry.

Take a look at this. Redbook (and to think I smirked at my mom for reading this magazine when I was a teenager) at https://www.redbookmag.com/body/healthy-eating/g2819/foods-that-make-you-hungry/?slide=1 explains about fruit making you feel hungrier:

“’Fruit juice may already be on your no-go list, but if you’re eating more than one serving of the whole variety (i.e. one banana or one cup of berries), you may want to scale back. It may have nutritional benefits, but fruit is not going to help suppress your appetite,’ says Perlmutter. ‘It contains both fructose and glucose, which won’t signal insulin, causing your appetite to rage on.’”

Perlmutter is David Perlmutter, MD, a board-certified neurologist and author of Brain Maker.

Got it: More fiber, less sugar. Now the only question is can I get myself to adhere to that… and can you if you choose to stop being hungrier after eating than you were before.

Talking about magazines, Arizona Health and Living at https://issuu.com/arizonahealthandliving/docs/arizona_health_and_living_magazine__9a2d374f4dffc2 is helping me spread awareness of Chronic Kidney Disease. This is in their June 2018 issue.

 

Guess what I found when I was preparing my non-CKD book for last Thursday night’s reading at our local The Dog Eared Pages Used Book Store. You’re right. It’s a copy of the newly minted (um, printed) SlowItDownCKD 2017. Would you like it? All that I require is your address and that you haven’t received a free book from me before.

Random thought: I cannot believe I just chose a Father’s Day gift for my son-in-law’s first Father’s Day. Add my youngest’s upcoming nuptials and this is a very happy world I live in. Here’s hoping yours is a happy one, too.

Until next week,

Keep living your life!