The problem isn’t eGFR per se. The problem is the inaccurate eGFR on the lab report, which is just inversely correlated with serum creatinine.
I had to explain all this to my primary care physician when I bulked up significantly, because she was convinced I was on the verge of kidney failure, and I was like “I did some reading. Please order cystatin C.” Then you can calculate your eGFR yourself using both datapoints. My cystatin-C only eGFR is nearly 2x my creatinine-only eGFR.
eGFR: 94 as of August 2024
age 70
Male
I haven’t started rapamycin yet but would like to soon. I was using compounded rapamycin and had several blood tests, each of which showed rapamycin below measurable levels, so I consider that as “haven’t started yet”. The multiple blood tests were of variations such as putting the compounded rapamycin capsule in other types of capsules including those advertised as acid-resistant, mixing rapamycin with a penetration enhancer and applying to skin, and dissolving under tongue.
My eGFR was not previously that high. I wonder if it’s higher this year because I started taking enzymes or apple cider vinegar.
Diet: no beef or pork. I probably don’t get enough protein.
eGFR (from standard blood test) 106
age 51
sex M
Also, if care to share:
Diet Mostly lean protein / non-starch vegetables; protein+fiber forward
Rapa user? 6mg/week
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cystatin-C 0.67 since it’s being discussed
Double check this but I think blood urea nitrogen (BUN) on your blood panel is a rough marker of protein intake. I eat nearly vegan diet, a little fish, and am also 70, but I don’t seem to have evidence of muscle loss. Probably because I exercise daily. BUN runs a bit low consistent with my diet which is clearly not high protein.
I didn’t know that, thanks for letting me know. My BUN is 15, which is within the reference range of 7-25 mg/dL. So maybe my protein intake is OK.
My glomerial filtration rate is 86 . I am 73yrs old 5’10 175lbs
I may be wrong, but from my novice understanding, and as someone with light CKD myself (IGA nephropathy), proteinuria is a more important factor in kidney decline than serum creatinine. My serum creatinine is transient and can get to negative numbers like over 1.3 (it can get much lower though, too). I think rapa might even play a role in serum creatinine temporary elevation, dont quote me there. But my proteinuria is very low, and there registers no protein or blood in urine on the general tests.
Doctors still use eGFR though
I can see that my sugar and obesity issues probably affecting my eGFR with a range from 68-90. I guess I know what I must do. LOL
Checking Cystatin C made a huge difference for me. My eGFR on my CMP was 67 but after the Cystatin C lab it came back at 101. 56y/o female.
I am wondering if you are taking supplemental creatine? Doing so will raise your creatinine level, but not the Cystatin C level. For this reason, creatine supplements should be avoided by those with CKD, as taking creatine will create confusion when creatinine levels are elevated. Monitoring Cystatin C can help clarify, but since it’s a more expensive test, doctors are reluctant to order it.
Can someone explain to me what Cystatin C is? What is it relative to eGFR? I am not sure if we have this blood test in Australia. I will find out next week.
A Simple Blood Test Mismatch May Predict Kidney Failure, Heart Disease, and Death
Google Gemini is your friend! 
This analysis compares Cystatin C testing with the standard eGFR (Creatinine) test, highlighting their mechanisms, clinical applications, and specific relevance to longevity and health optimization.
| Feature | eGFR (Standard / Creatinine) | Cystatin C |
|---|---|---|
| Source | Creatinine: A waste product of muscle metabolism (breakdown of creatine phosphate). | Cystatin C: A protein produced at a constant rate by all nucleated cells in the body. |
| Physiology | Filtered by kidneys; roughly 10-40% is also secreted by tubules (making it “dirtier” data). | Freely filtered by glomeruli; reabsorbed and catabolized by tubules (cleaner filtration marker). |
| Primary Variable | Muscle Mass. High muscle = high creatinine (low eGFR). Low muscle = low creatinine (high eGFR). | Cellular Turnover. Unaffected by muscle mass. |
| Equation | Typically calculated via CKD-EPI 2021 (creatinine-based). | Calculated via CKD-EPI 2012 or 2021 (cystatin-based). |
While Cystatin C avoids the muscle bias, it has its own confounders (though fewer):
For a specialist in longevity and healthcare, Cystatin C is the far more valuable metric for three specific reasons:
Studies consistently show that Cystatin C is a stronger predictor of all-cause mortality and cardiovascular events than Creatinine. Even in populations without kidney disease, elevated Cystatin C correlates with “Shrunken Pore Syndrome”—a pathophysiology where the kidney filters small molecules (creatinine) fine but struggles with larger middle-molecules (Cystatin C, 13 kDa), leading to the accumulation of atherogenic proteins.
Biohackers and longevity clinicians analyze the discordance between the two metrics:
Cystatin C levels correlate linearly with inflammation and arterial stiffness. It is effectively a “vascular health” marker masquerading as a kidney marker.
| Scenario | Recommended Test | Rationale |
|---|---|---|
| Annual Physical (General Pop) | Creatinine eGFR | Cheap ($15-$30), widely available, sufficient for average phenotypes. |
| Bodybuilders / Athletes | Cystatin C | Creatinine will be falsely elevated due to muscle turnover. |
| Elderly / Low BMI | Cystatin C | Creatinine will be falsely low due to muscle atrophy, masking kidney failure. |
| Longevity Protocol | Both | To calculate the discordance/gap and screen for “Shrunken Pore Syndrome.” |
| Strict Keto/Carnivore Diet | Cystatin C | High dietary protein intake elevates creatinine, skewing standard results. |
Given your occupation in Biotech/Longevity:
@RapAdmin Excellent explanation of the issue. I will again draw attention to the issue of Creatine supplementation (which presumably many here are using). These will lead to the measurement of high creatinine levels (as creatine is metabolized to creatinine), and diagnostic confusion as what the elevated levels are due to. This happened for myself, when I was thought to have CKD 2 (Cr 1.24, EGR 64). When I stopped supplementing Creatine, everything was once again within normal limits. Cystatin C can get around this, but as I mentioned earlier, doctors are reluctant to order it because it is more expensive. I prefer to avoid the confusion, and I avoid supplements with Creatine.
I’m actually no longer taking creatine. I think I probably got mildly dehydrated during a trip to a warmer climate where I did a lot of hiking at a high elevation. I didn’t eat or drink normally on the trip either fwiw. I was only 36 hours out from lifting as well.
Given creatine’s benefits (proven and unproven), it seems like not taking just because of a lab value seems like an overreaction.
I would presume someone has checked to see how much time to hold off on it before a blood draw to get it “out of your system”.
Truth be told, there is creatine in meat so most people are getting some anyway.
While kidney function correlates with lifespan, it mostly is just a marker rather than causative. When people die of kidney failure, it is usually in the setting of diabetes or poorly controlled hypertension and sometimes just multi organ failure which shows first in the kidneys.
Kidneys are fragile beasts and are relatively easy to quantify (compared to brain which is also fragile). So when people get sick, kidneys show it - sometimes for months. But nearly always, this is a result of something else not primary renal disease.
Some drugs are certainly nephrotoxic and then creatinine needs checked more often but for average person with good sugars and low BP, it isn’t needed very often.
I had blood work recently and I take 5-10 gm daily creatine. I held off for 72 hours. My cr was .73 and BUN was 28. So cr was lower end of normal but BUN was high. Over the last 5 years on no creatine, my cr was slightly higher and BUN never high. Go figure … And then I had another data point on creatine without stopping and cr was .83, BUN 21. There is enough fluctuation based on hydration and exercise that the creatine effect in me was zero.
Side note - for MDs this forum is a bit confusing because you have posters with incredible knowledge that don’t have some basics from medical school so hard to know what language is ok. I would say “kidney” to a patient but always “renal” to an MD.
As you have suggested to avoid diagnostic confusion prior to lab draws, the problem is that creatine slowly saturates muscles over time with continous daily supplementation. While serum levels will decline over a few days of cessation, the creatine that has saturated the muscle tissue will still be leaching out from the muscles. This could lead to diagnostic confusion even after a few days.
In my case, I take enough supplements, that this is one I am happy to avoid regardless of whether one can get around the confusion by cessation of supplementation for a few days.
I’m not sure I understand your comment about MDs, but I hope this forum will be welcoming to all regardless of background.
Age: 41, male
Weight: 157 lbs
Height: 5 foot 11 inches (BMI = 21.9)
Creatinine: 79, 69, 73 umol/L (over past 3 tests)
eGFR: 109, 114, 110 mL/min (over past 3 tests)
Diet is nearly 100% whole food plant based, with occasional fish (maybe 1-2x per month). Alcohol is limited at perhaps 5-10 drinks per year. Not a rapamycin user here.
Agreed. 3 days isn’t really enough to normalize things completely - hard to know exactly how much time would be needed because it would be individual based on muscle mass, diet, creatine dosage etc.
My experience with creatine made me a “believer” in supplements. Meaning that I was so impressed with it’s effects that I looked into others and am now taking a decent size stack when I took nothing before. I eat a decent amount of meat so I don’t really think I was “deficient”. Given that creatinine as a test is compromised so much anyway, I just don’t see the problem. Now, if someone has CKD, that is different. I suspect that annual tracking of creatinine if you stayed on a constant dose of creatine would be perfectly fine for most people. Just like it is fine for tracking a muscular person - we just mentally adjust it and trend it anyway. The analogy could go farther and say, would you avoid gaining muscle because it makes the creatinine higher? Now maybe creatine intake leads to greater variability in creatinine levels? For my N=1, creatine intake didn’t move the needle at all.
If you consider AD to be a problem at least partly related to starving neurons unable to use glucose well, then it would stand to reason that providing energy or ways of using energy to those neurons in anyway possible should help. I don’t pretend to know, but it makes intuitive sense to me (knowing full well how little that is worth).
My MD comment - this forum has MDs and other people with medical background and also very knowledgeable people without medical backgrounds. So it is unclear to me what level to post at without insulting anyone. Hence my using both renal and kidney terms when I should stick to one.