Creatine and Kidney Health: Clinical Evidence in Healthy Adults

Mention creatine to your doctor and there's a better-than-even chance they'll warn you about your kidneys. It's the most persistent safety concern in sports nutrition — repeated by clinicians, trainers, and media outlets for over two decades. The concern is understandable on the surface: creatine metabolism involves the kidneys, and one of its byproducts (creatinine) is used as a marker of kidney function. But the clinical evidence tells a different story entirely.

Multiple controlled trials, systematic reviews, and position statements from the ISSN and other sports nutrition organizations have examined renal function in creatine users. The consensus: creatine monohydrate at recommended doses does not impair kidney function in healthy individuals. The evidence is not ambiguous.

Where the Concern Originates

The kidney concern traces to two sources. First, a 1998 case report published in The Lancet described a man with pre-existing kidney disease (focal segmental glomerulosclerosis) who experienced a decline in renal function while taking creatine. This single case, in a patient with already-compromised kidneys, was extrapolated far beyond what the evidence supported. It became the foundation for a general claim that creatine harms kidneys, a conclusion the case report itself did not make.

Second, the relationship between creatine and creatinine creates confusion. Creatine is non-enzymatically converted to creatinine at a rate of approximately 1.7% per day. When you increase creatine intake, you increase creatinine production. Since serum creatinine is the most common screening marker for kidney function, supplementation can produce lab values that look abnormal to clinicians unfamiliar with this mechanism. The kidneys are not struggling to clear creatinine. There is simply more creatinine to clear because there is more creatine in the system.

The Poortmans and Francaux Data

The most directly relevant study addressing this question was published by Poortmans and Francaux in 1999 in Medicine & Science in Sports & Exercise. They studied renal function in athletes who had been using creatine for months to years. Their methodology was straightforward: measure actual kidney function (glomerular filtration rate, albumin excretion rate) rather than relying solely on serum creatinine.

Their findings: no difference in renal function between creatine users and non-users. The glomerular filtration rate, the gold-standard measure of how well the kidneys filter blood, was normal in both groups. Albumin excretion, a sensitive marker for kidney damage, showed no elevation. The kidneys were functioning identically regardless of creatine supplementation status.

This study was pivotal because it used the right markers. Serum creatinine alone can be misleading in creatine users, as explained above. By measuring GFR directly, Poortmans and Francaux bypassed this confound and assessed actual kidney function.

The Lugaresi Long-Term Study

Lugaresi et al. (2013), publishing in the Journal of Renal Nutrition, conducted a 12-week randomized, double-blind, placebo-controlled trial specifically designed to assess creatine's effects on kidney function. Participants received 10 g/day of creatine (a dose higher than the standard maintenance recommendation) for the full 12 weeks.

The investigators measured cystatin C (an alternative GFR marker unaffected by muscle mass or creatine intake), serum creatinine, blood urea nitrogen, urinary albumin, and calculated GFR. After 12 weeks of above-standard dosing, none of these markers showed clinically meaningful changes. Kidney function was preserved.

The inclusion of cystatin C was methodologically important. Unlike creatinine-based GFR estimates, cystatin C is not influenced by creatine supplementation, body composition, or dietary protein intake. It provides an independent assessment of kidney filtration. The fact that this independent marker confirmed normal function added substantial strength to the conclusion.

Additional Supporting Evidence

The Poortmans/Francaux and Lugaresi studies are the most cited, but they are far from alone. Multiple additional studies have examined renal function in creatine users:

Kreider et al. (2003) published long-term follow-up data on athletes who had supplemented with creatine for up to 21 months. Comprehensive metabolic panels, including renal function markers, showed no abnormalities compared to non-supplementing controls.

Gualano et al. (2008) specifically examined creatine supplementation in an individual with a single kidney, a population that would be expected to show vulnerability to any nephrotoxic substance. After 12 weeks of supplementation, kidney function remained normal. While a single case study cannot establish population-level safety, it further undermines the claim that creatine is inherently nephrotoxic.

Gualano et al. (2011) later studied creatine supplementation in type 2 diabetic patients, a population with elevated baseline risk for kidney complications. After 12 weeks of creatine supplementation combined with exercise training, no deterioration in renal function was observed.

The ISSN position stand (Kreider et al., 2017) reviewed the totality of this evidence and concluded that there is no evidence that creatine supplementation causes renal dysfunction in healthy individuals.

Understanding the Lab Work Confusion

A practical problem persists despite the clear research. Many physicians still use serum creatinine as a standalone marker when evaluating kidney health. The estimated glomerular filtration rate (eGFR) reported on standard metabolic panels is typically calculated using the CKD-EPI equation, which uses serum creatinine as its primary input. In a creatine user, this can produce a falsely low eGFR reading.

Here is what happens mechanistically: you take 5 g of creatine daily, your intramuscular creatine stores increase, the non-enzymatic conversion to creatinine increases proportionally, your serum creatinine rises, and the eGFR equation interprets this rise as reduced filtration. But the rise reflects increased creatinine production, not decreased creatinine clearance. The kidney is doing its job. There is simply more substrate to process.

If you supplement with creatine and your physician flags elevated creatinine or low eGFR, the appropriate next step is a cystatin C-based GFR measurement, which is independent of creatine metabolism. Alternatively, a 24-hour urine creatinine clearance test provides a direct measure of kidney filtration. Both will show normal function in a healthy creatine user.

The article on creatine and creatinine levels covers this topic in greater detail, including specific guidance for discussing supplementation with healthcare providers.

Pre-Existing Kidney Disease: A Different Question

The safety data discussed above applies to individuals with healthy kidneys. The question of creatine use in people with pre-existing kidney disease is separate, and the answer is more cautious.

Insufficient controlled research exists in populations with diagnosed kidney disease to make definitive safety claims. The 1998 Lancet case report involved a patient with existing nephropathy. While a single case cannot establish causation, it is reasonable to exercise caution. Individuals with chronic kidney disease, on dialysis, or with known renal impairments should consult their nephrologist before using creatine.

This is not because creatine has been shown to harm diseased kidneys. It is because the research has not adequately studied this question. Absence of evidence of harm is not the same as evidence of absence of harm, and responsible science requires acknowledging this distinction.

Summary of the Clinical Evidence

The kidney safety data for creatine monohydrate in healthy individuals includes:

Direct GFR measurements showing no difference between creatine users and non-users. Cystatin C measurements (independent of creatine metabolism) confirming normal filtration. Long-term studies up to 21 months showing stable renal function. Studies in at-risk populations (single kidney, diabetic patients) showing no deterioration. Position statements from major sports nutrition organizations confirming renal safety.

The claim that creatine damages kidneys in healthy people is not supported by any controlled study. It is contradicted by every controlled study that has examined the question. The persistence of this myth reflects the gap between research evidence and public understanding more than it reflects any genuine clinical concern.