Oct 11, 2026
You start taking creatine, continue training, and your next blood test shows a higher creatinine. The laboratory also reports a lower estimated kidney filtration rate. Did the supplement injure your kidneys?
Possibly, but those two numbers do not establish that diagnosis. Creatinine can increase because your kidneys are clearing less of it, because your body is generating more of it, or because both processes have changed. The job is to distinguish those explanations without dismissing a genuine kidney problem.
This is particularly relevant if you lift weights, carry substantial muscle mass, or use testosterone. A laboratory equation is useful, but it does not know your training history or what is in your supplement container.
Creatine and creatinine are related compounds, but they are not interchangeable. Creatine participates in the phosphocreatine system inside muscle. When a muscle contracts, adenosine triphosphate, or ATP, supplies energy and becomes ADP. Phosphocreatine can donate a phosphate group through the enzyme creatine kinase to regenerate ATP rapidly. This is one reason creatine supplementation can help repeated, high-intensity efforts.1
Separately, a portion of the creatine and phosphocreatine pool undergoes spontaneous conversion to creatinine. Creatinine enters the circulation and is removed mainly by the kidneys. More muscle generally means a larger source of creatinine. Supplementing creatine can also alter its production. Neither observation means that every creatine user develops a high result.
The laboratory's estimated glomerular filtration rate, or eGFR, often comes from an equation incorporating serum creatinine. Glomeruli are the microscopic filters in the kidneys. If creatinine increases, the calculated filtration estimate generally falls. That second number is therefore not independent confirmation that filtration has deteriorated. It is, in part, a mathematical consequence of the first number.2
There is another qualification: standard eGFR equations work best when the marker is reasonably stable. During a rapidly evolving kidney injury, today's creatinine may not yet reflect today's filtration. An apparently modest change still deserves attention when the clinical picture suggests an acute problem.
A useful experiment measures kidney filtration with something other than creatinine. In a randomized trial published in 2013, resistance-trained men taking creatine monohydrate received 20 grams daily for five days, followed by five grams daily over a 12-week study. The participants were already eating relatively high-protein diets.3
The investigators used chromium-51-labelled EDTA clearance, an external filtration tracer. Unlike creatinine, that tracer is not generated by your muscles. They found no significant difference in the change in measured filtration between creatine and placebo. Urinary albumin and protein also did not show a harmful treatment effect.
That is reassuring within the conditions tested. It is not proof of unlimited safety. Forty-six men were randomized, but only 26 completed the analysis: 12 receiving creatine and 14 placebo. The study was designed to detect a relatively large, 20 percent reduction in filtration. Its size, attrition, and three-month duration limit what it can exclude, particularly rare injury or smaller long-term effects.
A second randomized study, published in 2020, analyzed 30 healthy men, ten each receiving placebo, three grams, or five grams of creatine monohydrate daily for 35 days. It examined conventional kidney tests and urinary markers of tubular injury and inflammation.4 These additional markers address a different question from whether a muscle-derived waste product has risen. No statistically significant increase was detected in the exploratory markers, KIM-1 and MCP-1. The investigators did not measure filtration with a tracer or obtain cystatin C. Again, a small, short study cannot establish that an adverse reaction never occurs.
The larger literature points in the same general direction, with an important distinction. A 2026 meta-analysis of randomized studies found an average serum creatinine increase of 0.13 milligrams per decilitre with supplementation. It found no statistically significant difference in estimated filtration.5 That average increase is not a correction factor to subtract from your own result. Individuals, formulations, doses, and study methods differ, and the pooled filtration estimate was imprecise.
One paper in the Man Medicine research library describes a man whose creatinine rose substantially while he was taking creatine ethyl ester, then returned toward normal after the supplements were stopped.6 The authors concluded that the supplement had produced a misleading picture of impaired filtration.
Creatine ethyl ester is not creatine monohydrate. The ester can convert to creatinine before absorption, increasing the circulating marker without necessarily reducing actual kidney filtration. This published case illustrates a diagnostic trap. It does not tell us how frequently that happens, and it should not be presented as a trial of ordinary monohydrate use.
So the history needs to be specific. “I take creatine” is the beginning of the discussion. Which form? How much? For how long? Is it a single ingredient or a mixture? What else changed before the blood draw?
The same distinction applies to muscular men using testosterone. A 2024 retrospective study in the research library examined creatinine and cystatin C in 227 male athletes reporting testosterone use.7 The two markers showed differing relationships across body-composition groups. That supports questioning whether creatinine alone adequately describes renal function in this population.
But the study did not measure filtration with an external reference tracer. It cannot prove that cystatin C was the correct answer in every participant. Nor does comparing two blood markers demonstrate that testosterone is harmless to the kidneys. These were observations at one centre, not a randomized renal-safety trial.
Muscularity can explain part of a creatinine result. It cannot automatically explain a sudden rise, albumin leaking into the urine, new hypertension, or an ongoing downward trend in kidney function. Being strong does not make you immune to kidney disease.
Cystatin C is a small protein produced by nucleated cells and filtered by the kidneys. It is less dependent on skeletal muscle mass than creatinine. Measuring it can help when a creatinine-based estimate seems inconsistent with the person in front of you.2
Less dependent does not mean unaffected by everything else. Thyroid dysfunction, glucocorticoid exposure, inflammation, and other non-filtration factors can influence cystatin C. Choosing whichever marker gives the more reassuring answer is not a sound diagnostic strategy.
The current KDIGO chronic kidney disease guideline recommends the combined creatinine–cystatin C estimate when creatinine alone is less accurate and the result influences clinical decisions. For an otherwise healthy person whose increased muscle mass is the only relevant abnormality, a cystatin-C-only estimate can also be useful. If the estimates remain uncertain and the consequence is substantial, measured filtration may be appropriate.8
That last step is especially relevant when a result will determine a consequential medication dose or another decision requiring greater precision. Most people do not need a filtration-tracer study simply because one routine result is slightly outside its reference interval.
There are published reports of genuine kidney injury in people taking creatine. A 2012 report described biopsy findings consistent with interstitial nephritis, inflammation in the tissue surrounding the kidney tubules, after creatine monohydrate use.9 The patient had substantial illness and other abnormal findings, not merely an isolated laboratory flag.
A single case cannot calculate the risk or establish that pure creatine was the sole cause. Nevertheless, it prevents an honest review from saying that every adverse report is just creatinine production. Randomized trials and case reports answer different questions: trials estimate treatment effects under controlled conditions; case reports can identify events that deserve investigation.
Existing kidney disease, unexplained abnormal tests, or an acute illness changes the discussion. Do not extrapolate results from healthy lifters to advanced kidney disease. A clinician should review supplementation in that setting, including medications, dehydration, and potentially kidney-harming exposures such as frequent nonsteroidal anti-inflammatory drug use.
First, establish the trend. Compare the result with previous measurements and identify when supplements, training, illness, or medications changed. A stable baseline and a rapid increase are different clinical situations.
Second, tell the clinician exactly what you take. Bring the ingredient label and the dose. Include prescribed testosterone, nonprescribed hormones, pain medicines, and other supplements. A large cooked-meat meal and strenuous exercise around the time of testing can complicate interpretation. Follow the clinician's instructions about repeat testing; do not stop prescribed medicines or force excessive water intake to produce a better number.2,6
Third, evaluate more than filtration estimates. Blood pressure, urine albumin-to-creatinine ratio, urinalysis, electrolytes, symptoms, and the broader medical history help determine whether there is evidence of kidney disease. A normal urine test is reassuring in context, but does not exclude every kidney disorder. Cystatin C can resolve some uncertainties; it does not replace the rest of the assessment.8
Finally, separate chronicity from urgency. Chronic kidney disease requires abnormalities persisting for at least three months, or other evidence establishing chronicity. That does not mean waiting three months to investigate a new abnormality. Rapidly rising creatinine, markedly reduced urine output, swelling with breathlessness, or severe muscle pain or dark urine after exertion warrant prompt medical assessment.8,10,11
The practical conclusion is straightforward. A higher creatinine after starting creatine may reflect altered marker production rather than damaged kidneys. Confirm that explanation instead of assuming it. Use the trend, the urine findings, the clinical context, and, when needed, a second filtration marker to decide what the number actually represents.
1. Kreider RB, et al. International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine. J Int Soc Sports Nutr. 2017;14:18. https://doi.org/10.1186/s12970-017-0173-z
2. Pasala S, Carmody JB. How to use... serum creatinine, cystatin C and GFR. Arch Dis Child Educ Pract Ed. 2017;102:37–43. https://doi.org/10.1136/archdischild-2016-311062
3. Lugaresi R, et al. Does long-term creatine supplementation impair kidney function in resistance-trained individuals consuming a high-protein diet? J Int Soc Sports Nutr. 2013;10:26. https://doi.org/10.1186/1550-2783-10-26
4. Vilar Neto JO, et al. Novel renal biomarkers show that creatine supplementation is safe: a double-blind, placebo-controlled randomized clinical trial. Toxicol Res (Camb). 2020;9:263–270. https://doi.org/10.1093/toxres/tfaa028
5. Tsiaras A, et al. The Effect of Creatine Supplementation on Kidney Function: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. J Ren Nutr. Published online April 24, 2026. https://doi.org/10.1053/j.jrn.2026.04.010
6. Williamson L, New D. How the use of creatine supplements can elevate serum creatinine in the absence of underlying kidney pathology. BMJ Case Rep. 2014. https://doi.org/10.1136/bcr-2014-204754
7. Ashouri R, et al. Creatinine and Cystatin C: A Measure of Renal Function in Men With Testosterone-Induced Muscle Hypertrophy. Am J Mens Health. 2024;18. https://doi.org/10.1177/15579883241286654
8. KDIGO. 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(Suppl 4S):S117–S314. https://kdigo.org/wp-content/uploads/2024/03/KDIGO-2024-CKD-Guideline.pdf
9. Ardalan MR, Samadifar Z, Vahedi A. Creatine monohydrate supplement induced interstitial nephritis. J Nephropathol. 2012;1:117–120. https://doi.org/10.5812/nephropathol.7530
10. NHS. Acute kidney injury. Reviewed March 2026. https://www.nhs.uk/conditions/acute-kidney-injury/
11. CDC/NIOSH. Signs and Symptoms of Rhabdomyolysis. https://www.cdc.gov/niosh/rhabdo/signs-symptoms/index.html
Educational information, not an individual diagnosis or treatment plan.
