Creatine and Creatinine are 2 different things.
Creatine is a useful energy compound your body stores in muscle to help generate quick power. It can also be taken as a supplement.
Creatinine is a waste product created when creatine is broken down. Your kidneys filter it out, so it’s used as a marker of kidney function in blood tests
You can measure Cyctatin C for kidney function instead of measuring Creatinine.
Thanks for the explanation but I was under the impression that once I start using Creatine which is what I meant and will fix my post above(i plan on taking 4-5g daily) my eGFR number will decrease and may not be a good indicator of kidneys health. Or not necessarily? I just happen to be very sensitive about my kidney’s health more so than that of other organs perhaps and I don’t even have a good answer why (lol). So, if I knew for sure that creatine is bad for kidneys’ I’m actually fine with not doing creatine at all even though its benefits are always noted by longevity docs.
If you start taking Creatine your eGFR number will decrease. Creatine supplementation will trigger false alarms. It will convert into Creatinine in your body, making Creatinine number higher which will affect eGFR calculation. I have reduced kidney function due to transplant so I don’t want to overload my kidney with additional Creatinine to process. Kidneys will have to work harder to excrete additional Creatinine. For healthy kidneys it’s OK. So your decision depends on overall health of your kidneys.
Age: 51
eGFR: 89
Rapamycin 4mg a week with GFJ
If there were any doubt about the impact of creatine on eGFR: according to my more recent labs, my creatinine based eGFR is 63, and my cystatin-C based eGFR is 98.
I am not a nephrologist, but I work with several and I am good friends with one. So here are some things I I’ve learned.
In an elderly person with low muscle mass, they have a nice low creatinine, resulting in a high eGFR (especially when adjusted for their body weight), and that masks their poor kidney function. There also used to be a “racial” adjustment factor, based on the idea that people of African origin carried more muscle mass, which I think was removed from guidelines. And that was basically masking poor kidney function in those people. However, there are actually some differences between ethnicities. Japan applies a multiplier of 0.8, for example, in recognition of their population generally being lower BMI, less muscle, and that the normal equation again masks declining kidney function.
I also learned that cystatin-C isn’t perfect either. It’s affected by inflammation, thyroid activity and obesity.
Basically, if kidney function really matters, then you need to directly measure it with clearance tests where they give you a contrast agent and you collect urine over time to measure actual GFR. (I’m sure @LaraPo would have done before!) But it’s rarely done outside of research labs or very serious conditions (transplants, dosing chemotherapy etc)
I consider these blood tests as something for monitoring, since you need pretty dramatic changes to cause alarm. For example, here are my readings over the last 10 years:
So, biological CV% is around 5%, analytical CV% of the assay is around 3% at a good lab. So combining these together equates to expected variations of ~7% when measuring creatinine.
Add onto that the “reference change value” which is the way to detect what is measurement noise versus a real change. For my numbers, that would be around 16.6%. For me, that would mean a result outside of 0.83 or 1.15, which is a pretty huge range.
For acute kidney injury, an increase of >0.3mg/dl within 48 hours, or 1.5X your baseline over 7 days would be an indicator that something bad has happened.
Aside from that, I don’t think these values are super useful for anything except long-term monitoring. I wouldn’t take great faith in them being “normal”. You can also see that my own creatinine is slightly falling on average over 10 years, which is the opposite of what we’d expect with ageing. But all of it is still totally within normal parameters, so I don’t get excited either way.
45 y/o male
eGFR 100 avg over two years
Cystatin C 0.67
Vegetarian
No rapa
Creatine 5g/day (skip two days before testing)
Telmisartan 80mg
Something else that can skew your score is a vigorous workout within a few days of your test, as I learned from @Davin8r and then verified empirically. This affects the creatinine score but not the cystatin-C.
People also need to remember that creatinine metabolises in blood samples. Hence the time between blood draw and testing is a material issue as if you wait a day you will get perhaps 10 micromolar higher creatinine.
My last blood test uniquely for Randox produced results in under 24 hours so I know the creatinine was tested in less than 24 hours and was 77 micromolar (which is an eGFR of 95 according to the Lab’s algorithm). My test the two weeks before were 91 and 96 (80 and 76), but that was Medichecks which goes in the post hence the test was over 24 hours. The week before was 84.7 (eGFR 88) that was Randox, but the test was slower.
My best results for creatinine (61.82, 64.36, 67.83 - 2022) were from lab which did the tests immediately after the blood draw. I have not used the lab for a while because they got stressed with me turning up with my own blood. My worst result (122 egfr 54) were from a lab where I was worried about this issue and did two blood draws from the same needle and sent the second test to medichecks which although it was in the post gave the result 85.64.
I have a rule of thumb of 10 micromolar for each day of testing delay.
I was getting some really good Cystatin-C results, but those seem to have gone a bit awry. However, I am not worrying about it because when you look at the results in the round my kidney function is OK. I will at some stage have another look at what I can do with Cystatin-C as I would like to know why this is, but it is not a priority in my test cycles.
10 micromolar is about 0.11 mg/dL
Yes, I am mindful of the time lapse. Labcorp seems to have more of a backlog than my local hospital, though even there the waiting rooms are often jammed.
59 y.o. male
eGFR- creatinine - 102
eGFR -cystatin C - 78
According to Gemini, my relatively poor cystatin c is due to low ferritin 11 (which I have now bumped up to 31), and dehydration.
That’s an interesting point. I have just asked Gemini about links between cystatin C and ferritin and it did not give an answer that would imply a low ferritin would result in a high cystatin C. Do you have any further from gemini on this.
Here’s a blurb from Gemini:
Your Hematocrit of 48.5% combined with a Ferritin of 11 suggests your body is in a state of “stress erythropoiesis.”
We previously looked at SOD2 TT and viscosity. Now we have a structural cause: Iron Deficiency.
There are various parts of that that don’t seem right. Simple things like the claim that the kidneys are the most energy demanding cells. I thought a simple solution to this was to ask Gemini for a review of what Gemini said and I copy that below. It appears, for example, that it is actually that renal tubules are mitochondria dense rather than energy demanding.
This academic review examines the provided statements regarding the “Pseudo-High Hematocrit Paradox” and its proposed link to Cystatin C levels. The theory attempts to bridge hematology, renal physiology, and mitochondrial bioenergetics.
The core of this argument rests on the rheology (blood flow characteristics) of iron-deficient erythrocytes.
This section moves from mechanical explanations to metabolic ones, which generally have stronger footing in molecular biology.
Mitochondrial Bioenergetics: The statement regarding the Electron Transport Chain (ETC) is highly accurate. Iron is a mandatory cofactor for Heme-containing proteins and Iron-Sulfur ($Fe-S$) clusters in Complexes I, II, and III. The renal tubules are among the most mitochondria-dense tissues in the body; “starving” them of iron impairs ATP production.
The SOD2 TT Interaction: This is a sophisticated integration of genomics. The SOD2 (Superoxide Dismutase 2) enzyme, specifically the $Val16Ala$ (TT) polymorphism, is associated with less efficient clearing of superoxide within the mitochondria.
If iron deficiency causes “electron leakage” in the ETC, it increases ROS (Reactive Oxygen Species) production. In an SOD2 TT individual, this creates a “double-hit” scenario where oxidative stress is elevated while the primary defense mechanism is compromised.
Cystatin C as a Marker: Cystatin C ($1.0\text{ mg/L}$) is often used as a more sensitive marker of GFR (Glomerular Filtration Rate) than creatinine. While $1.0$ is often at the top of the “normal” clinical range, in functional medicine, it is frequently viewed as a precursor to early renal strain. The theory that “internal pressure” or mitochondrial fatigue raises Cystatin C is plausible, as GFR is an energy-dependent process.
[ul]
[li]Scientifically Strong: The link between Ferritin of 11, mitochondrial ETC dysfunction, and SOD2-mediated oxidative stress.[/li]
[li]Plausible but Speculative: The idea that the body “chooses” a higher Hematocrit to compensate for iron-deficient cell “stiffness.”[/li]
[li]Non-Traditional: The “mechanical friction” explanation for Cystatin C. A more standard academic view would attribute this to ischemia-reperfusion-like stress caused by poor microcirculation and oxygen delivery.[/li]
[/ul]
The theory effectively identifies a “physiological bottleneck”: you have enough red blood cells (high Hematocrit), but they are functionally “hollow” or “rigid” due to low iron. This forces the kidneys to work harder in a high-oxidative-stress environment, potentially reflected in the elevated Cystatin C.
Would you like me to look into specific dietary or supplemental strategies that address the mitochondrial iron-oxygen-SOD2 triangle?
Do you have your figures for MCV and Hb?
Ya, I use the free version of Gemini and have found it to be a bit off at times. I have been running some of its responses through Claude, which tempers some of G’s claims.
2 months ago:
MCV - 93
Hb - 16
Ferritin - 11
Hematocrit - 48.3
Last week, after an iron protocol:
MCV - 93.3
Hb - 14.3
Ferritin - 31
Hematocrit - 45.3.
I plan to raise ferritin to 50-70 to see if it improves certain blood biomarkers as well as increases energy and endurance.
Those MCV values are not particularly low. It will, however, take a while for MCV to shift as RBCs last about 3 months.
Why was the ferritin so low?
Likely too many iron blockers and chelators: coffee until noon, yogurt throughout the afternoon, cocoa powder, berries, turmeric, high-phytate grains, metformin, high-dose melatonin. Barring that, occult blood loss? Had colonoscopy last year where inflammation detected at the juncture of the small and large intestines.
