No, I have never been diagnosed with protein in my urine
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Sounds like you may be in better shape than you thought!
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Yes, but frustrating that the doc could have done the cystatin C instead of me ordering for myself and doing this legwork. Why wouldn’t a nephrologist in 2020 not get a cystatin C level? I have been avoiding red foods for no reason based on his advice and thinking that my kidneys are slowly dying . Im a 6’6" muscly guy, not flabby, why wouldn’t they do that? Alright, I will pull myself together 
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Time for a new doc it seems
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A uACR test is preferred over basic urine dipstick to evaluate for possible early CKD (in consideration with eGFR). The National Kidney Foundation states the following on their website:
"A routine dipstick is not sensitive enough to detect small amounts of urine protein. Therefore, it is recommended that screening in adults with CKD or at risk for CKD be done by testing for albuminuria.
Albumin-to-creatinine ratio (ACR) is the first method of preference to detect elevated protein. The recommended method to evaluate albuminuria is to measure urinary ACR in a spot urine sample."
Marek Health offers this test for $25.
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I don’t believe I had the uACR but:
Urine Protein Creat Ratio 0.07
M Protein Ur-mCnc 9.3 mg/dL
Both values appear to be WNL
Thanks
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Notes from my interview with kidney doc Rick Johnson. He also talked about how to avoid Alzheimer’s.
What causes kidney disease?
- High sugar diets / Metabolic syndrome / Diabetes (cut back on sugar in food)
- Gout / High Uric acid: stay hydrated, avoid fructose (sugar is ½ fructose), minimize the purines (beer, shellfish, sardines, processed meats, gravy, bacon), take vit C (500 mg / day), quercetin, watch certain diuretics, SGLT2 inhibitors lower uric acid
- “Aging” (of kidneys) may be related to high sugar or high glycemic index carbohydrate diets
- High blood pressure is a kidney killer
- Avoid NSAIDs (ibuprofen is bad for kidneys; aspirin and Tylenol are okay)
- Proton Pump Inhibitors (PPI) cause multiple problems
- Avoid Dehydration (drink 8-10 glasses of water every day, and drink before consuming salty foods). Don’t drink too much too fast, especially after getting behind (being dehydrated).
- Spikes in blood sodium leads to temporary increases in BP which can progressively develop damage in the kidneys.
I hope this is helpful info.
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Get screened
Because CKD is often symptomless, it’s often undiagnosed. Screening tests are critical — at least once a year if you’re older than 60 or have high blood pressure or diabetes, Thavarajah suggests.
A routine blood test can measure levels of creatinine, a waste product from your muscles, to determine how well your kidneys are functioning. These test results can be combined with factors such as age, race and gender to determine your glomerular filtration rate (GFR). The lower it is, the more likely it is that you have CKD. Your doctor may also order a urine test to screen for a protein (albumin), which can be an early sign of declining kidney function, Thavarajah says — sometimes before anything shows up on a blood test.
Full article here: How to keep your kidneys working well (Washington Post)
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Kidney disease doesn’t get the attention it deserves. The I wonder why the mainstream medicine doesn’t shift to Cystatin-C (from creatinine) for a clearer signal?
Creatinine confounders: High / low muscle mass, Creatine supplementation
“Similarly, the present study also revealed that cystatin C is found to be more accurate than creatinine in estimating GFR with 96.8% sensitivity, compared with a sensitivity of 61.3% for creatinine in patients >60 years. “
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My doctor didn’t even know what cystatin-c was when I asked about it. I was worried about a drop in eGFR to 80ish after starting TRT and increasing protein and strength training, so I finally got cystatin-c tested.
When I plugged my numbers into the National Kidney Foundation calculator, adjusting for body surface area, my eGFR was 119. A huge difference!
In addition to creatinine being a poor measure, doctors rarely adjust the lab numbers for eGFR to reflect body surface area. You can’t just read the number off the lab report as it is. How do doctors not know this or not care?
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I haven’t confirmed with Labs, but I’m almost certain that my kidney function has improved with Rapamycin use. I’ve seen huge reductions in chronic inflammation as well as improved aerobic capacity with my heart function. I’m taking 8mg/Once weekly of Rapamycin Sirolimus tablets+Acarbose 50mg 3x daily, Metformin 500mg 2x daily witg breakfast and dinner(fat loss).
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Well I think docs and the labs do use the same eGFR calculator that you linked to. However, I don’t think that they usually adjust for the surface area or the muscle mass. That said the calculator seems to use your chronological age as a proxy for a muscle mass and activity level? Frankly I’m astounded that the muscle mass is not measured directly and be an optional input into this calculator. So all that said let’s just for fun go through little thought experiment with this NKF eGFR calculator. Let’s say you started exercising and taking rapamycin or some other yet to be invented but very successful anti-aging treatment. As a result you lost 20 pounds of fat and replaced it with muscle. You look and perform on every physical test like a person 30 years younger except of this kidney function calculator. Why so? Well your creatinine levels have not lowered much if at all as you are much more muscular now. Further with your new found energy you tend to move a lot more than before, which will increase your blood serum creatinine levels too. In summary to me this kidney calculator can be a useful tool but sometimes as counterproductive as BMI calculator.
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In med school they taught me that you need to correct the eGFR from creatinine for musculature and exogenous creatine intake, maybe these doctors didn’t pay attention…
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I was speaking to nephrologist who was not a fan of Cystatin-C, but I have not found out myself what the issues are with it. To some extent therefore, I am simply assuming that it is better than creatinine because I don’t know any reason why it would not be and I know lots of things that are wrong with creatinine.
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In 1991 when I graduated, they were not teaching about Cystatin-C yet. I am also finding out that much of what I was taught in Med school is turning out to be wrong, notably the food pyramid.
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Yes, that was me last year, which is why I finally just ordered cystatin-c to see where I really was.
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Hopefully not an overstep, but i remember before the standard was changed (in 2021) there was a regularly reported eGFR for african Americans listed with the overall eGFR results. The reasoning was “more muscle mass”, and was based on past observational studies (ie I believe researchers noticed a difference in creatine based eGFR and tried ti ascertain a reason). So following this logic, if you are more muscular, your creatine-based eGFR should be lower than if you looked like David Sinclair. I don’t believe cystatin based eGFR is impacted by muscle mass )or creatine levels) so there should be no difference. Also i recall cystatin based eGFR tests are waaaaaaay more expensive than creatine, and not covered by most insurance (what my docs have said, even though i have one kidney).
Race was originally included in eGFR calculations because clinical trials demonstrated that people who self-identify as Black/African American can have, on average, higher levels of creatinine in their blood. It was thought the reason why was due to differences in muscle mass, diet, and the way the kidneys eliminate creatinine.
This review focuses on potent antioxidants such as sulforaphane (SFN), N-acetyl cysteine (NAC), resveratrol, curcumin, quercetin, and α-mangostin in the improvement of mitochondrial function in kidney pathologies.
Antioxidants targeting mitochondria function in kidney diseases
Kidney diseases are a growing health problem worldwide, causing millions of deaths. Acute kidney injury (AKI) commonly evolves into chronic kidney disease (CKD) and fibrosis, which is a feature of CKD predisposing to end-stage renal disease. Thus, treatments that avoid this transition are urgently necessary. Mitochondria are the hub energy house of the renal cells, which provides energy in adenosine triphosphate (ATP) form, commonly obtained from β-oxidation through fatty acids degradation into the mitochondrial matrix. Mitochondria are plastic organelles that constantly change according to the cell’s energy requirements. For this, mitochondria carry out biogenesis, fission, fusion, and mitophagy/autophagy, processes highly regulated to maintain mitochondrial bioenergetics and homeostasis. Alterations in one or more of these processes might cause detrimental consequences that affect cell function. In this sense, it is widely accepted that mitochondrial dysfunction associated with oxidative stress plays a crucial role in developing kidney diseases. Therefore, antioxidants that target mitochondria might be an excellent strategy to ameliorate mitochondrial dysfunction, and selecting one or another antioxidant could depend on AKI or CKD requirements. This review focuses on potent antioxidants such as sulforaphane (SFN), N -acetyl cysteine (NAC), resveratrol, curcumin, quercetin, and α-mangostin in the improvement of mitochondrial function in kidney pathologies.
https://www.sciencedirect.com/science/article/pii/S259027922400004X
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Three of the things reviewed are also HDAC inhibitors.
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