Supplements · Metabolic & Cardiometabolic
creatine does not harm kidney function
In plain terms: Does creatine damage your kidneys?
Strong support Supplements 💰 Industry COI noted
Part of: 🧪 creatine
RefutedContestedStrong support
consensus score 0.80
No — not in healthy people at normal doses. Creatine nudges up a blood marker (creatinine) that can look like kidney trouble on a test, but meta-analyses and even genetic studies find no actual harm. Existing kidney disease is a separate conversation with your doctor.
📅 Last reviewed: 2026-07-14 ⓘ
Evidence ladder
How far up the ladder this claim has climbed. A high consensus on a low rung means "consistent so far," not "proven in people."
Top evidence so far: All trials, pooled (Meta-analysis)
MechanismIn-vitroAnimalObservationalRCTMeta-analysis
How the studies fall
4 support 0 contradict 0 tested null 1 mixed · 5 sources, 4 independent groups
What the evidence shows
The kidney-damage fear rests on a lab artifact: creatine raises serum creatinine (a harmless breakdown product), which inflates estimated GFR without any real loss of kidney function. Meta-analyses, an RCT, and a Mendelian-randomization study find no renal harm in healthy people at recommended doses. (Established kidney disease is a separate question, not tested here.)
The evidence (11)
| Source | Grade | Stance | Quality | Finding |
|---|---|---|---|---|
| Poortmans, Francaux 2000 · Sports Med. 2000 Sep;30(3):155-70 | observational | supports | low | Review: no evidence creatine damages kidneys in healthy individuals at recommended doses. |
| Al-Humadi S et al 2026 · Cureus | observational | supports | low | Narrative review for orthopedic surgeons states creatine's most common side effect is weight gain and there do not appear to be adverse effects on renal function in healthy athletes. |
| Zhou B, Hong M, Jin L, Ling K 2024 · Renal Fail | observational | supports | low | Two-part null. (1) Cross-sectional survey of 1,129 Chinese gym-goers (92% male; ~286 creatine users): 'Chi-square analysis revealed no significant association between creatine usage and renal function among the participants' (chi-square 0.96, p=0.619) - but the renal outcome is self-reported, which the authors concede 'inherently carries limitations due to its reliance on respondents' subjective feelings and personal health awareness'. (2) Two-sample MR on six renal biomarkers (serum creatinine, eGFR, uric acid, urinary microalbumin, urinary enzymatic creatinine, BUN): IVW 'did not demonstrate a significant correlation between creatine levels and the risk of six indicators evaluating renal function', all p>0.05, with no heterogeneity (Cochran's Q), no MR-Egger intercept pleiotropy and no MR-PRESSO outliers. Three reasons this is a weak null rather than a strong one: the MR exposure is genetically-predicted ENDOGENOUS creatine level, not supplementation, and its instrument GWAS has n=291 with 114 SNPs taken at p<1e-5 (winner's-curse territory that an F>10 filter does not fix); the microalbumin outcome GWAS is ukb-e-30500_AFR, an African-ancestry UK Biobank subset (n=3,036), against a European-descent exposure; and not one beta, OR or confidence interval appears in the readable text - every estimate sits in Supplemental Tables S1-S5 and in Figure 1, an image. In the paper's favour, the null is against its own stated prior ('we hypothesized that creatine supplementation might adversely affect renal function'), and funding is public (Zhejiang provincial health/TCM grants) with 'The authors declare no conflict of interest.' |
| Rubinchuk A et al 2026 · Cureus | observational | supports | low | Qualitative systematic review of 5 studies (3 RCTs + 2 cohorts) in under-18s — 3 of them clinical populations (juvenile dermatomyositis x2, SSRI-resistant depression) rather than healthy athletes. On the renal question: 'Across randomized controlled trials in pediatric and adolescent populations, no clinically meaningful changes were observed in serum creatinine, estimated glomerular filtration rate (eGFR), or other renal biomarkers'; 'No serious adverse events were attributed to supplementation.' Weight is limited: 'A quantitative meta-analysis was not performed due to the small number and heterogeneity of included studies', 'A formal risk-of-bias or methodological quality assessment ... was not performed', no PROSPERO registration, and 'The search strategy was limited to a single database (PubMed)'. The hepatic data come from one uncontrolled cohort and the cardiometabolic data from self-reported 'legal performance-enhancing substance' use, which the authors disown as creatine evidence: 'As exposure was not specific to creatine monotherapy and relied on self-reported data, causal inference regarding creatine alone is limited.' |
| Longobardi I, Solis MY, Roschel H, Gualano B 2025 · Frontiers in Nutrition | observational | supports | low | Short narrative review (Frontiers in Nutrition 2025), section 3. Verdict on the claim: 'available literature consistently shows that creatine monohydrate is safe when taken at recommended doses, even in clinical populations', and the claim's own mechanism is stated outright — 'individuals taking creatine supplements may naturally have higher serum Crn levels, without having any impairment in renal function'. Evidence behind it: the Poortmans series (1-80 g/day, 5 days to 60 months) where 'Their findings consistently showed no evidence of renal function impairments based on several parameters'; the authoring group's own trials in at-risk populations (single kidney, type 2 diabetes, rheumatic disease, pre-frail/frail elders) measured on Crn-independent biomarkers 'including the 51 Cr-EDTA clearance, which is considered a gold-standard technique for measuring GFR'. Table 1 grades kidney function 'Not supported / Grade I'. THREE CAVEATS THE PRIOR EXTRACT OMITTED. (1) Generalisability, in the authors' words: 'participants in all studies were predominantly healthy young men, which limits the generalizability of the findings'. (2) Non-independence: much of the renal evidence is the reviewers' own — 'We have found no evidence of renal impairment, even in clinical populations' — so this is a Gualano/Roschel (USP) restatement, not a fresh dataset. (3) Manufacturer COI: 'AlzChem provided financial support for the article processing charges (APCs)' and the senior author 'served as a member of the Scientific Advisory Board for Alzchem'. The review still bounds itself: 'Individuals with pre-existing kidney conditions should be monitored closely, as evidence is incipient and limited in this population.' |
| Vega, Huidobro E 2019 · Rev Med Chil | observational | supports | low | Review: creatine transiently raises serum creatinine, mimicking — but not causing — kidney disease. |
| Almeida 2020 · J Sports Med Phys Fitness | RCT | supports | low | Double-blind placebo-controlled trial, ~18 resistance-training males on creatine monohydrate 0.3 g/kg/day for 7 days vs dextrosol placebo: 'Blood and urine samples were collected pre- and 30 days post-supplementation to evaluate 41 biochemical parameters and renal function' and 'No modification of red blood cells parameters, white blood cells profile, blood lipid profile, metabolic and urine markers, hepatic and renal function were observed in the supplemented group.' A clean renal null, but the abstract reports no creatinine, eGFR or albuminuria value at all — no numbers anywhere in the paper's public text. Quality low: n~18, 7-day exposure, single post sample whose timing ('30 days post-supplementation') may sit weeks after the course ended. |
| Tsiaras A et al 2026 · J Ren Nutr | meta-analysis | supports | moderate | Systematic review + random-effects meta-analysis, 19 RCTs + 1 double-blind randomized crossover trial. Creatine raised serum creatinine (MD 0.13 mg/dL, 95% CI 0.07 to 0.18, n=19) with no difference in urea (MD -0.60 mg/dL, 95% CI -2.15 to 0.96, n=12) or eGFR (MD -5.20 mL/min/1.73 m2, 95% CI -15.00 to 4.60, n=8); no <1-month vs >1-month subgroup difference (Crn p=0.15, urea p=0.15, eGFR p=0.88). Quality moderate, not high: the eGFR null is pooled from only 8 trials and its CI spans -15.00 to +4.60 mL/min/1.73 m2, so it cannot exclude a clinically meaningful decline, and the authors conclude 'Further long-term RCTs, extending beyond one year, are needed to assess its safety in terms of renal function.' Heterogeneity, risk-of-bias, GRADE certainty and funding are not reported in the abstract (full text not available). |
| Naeini 2025 · BMC Nephrol | meta-analysis | supports | low | SR+MA 2025 (21 studies reviewed; creatinine pool 14 rows / 12 studies, GFR pool 5 studies, 69 vs 74 participants): GFR did not move - 'The meta-analysis revealed a non-statistically significant differences in GFR following creatine supplementation compared to control.' (Fig. 6: MD 3.15 [-4.97, 11.26], p = 0.45, I2 33%) - while serum creatinine rose trivially (MD 0.07 [0.01, 0.12], p = 0.03), read by the authors as 'statistically significant but physiologically benign, reflecting sustained creatine turnover rather than impaired kidney function.' Quality low, not moderate: no registered protocol, no certainty-of-evidence rating, a unit-of-analysis error (Kreider's single 44-person control group enters the pool three times, which is how control n reaches 263 vs 177 treated), self-contradictory study counts ('12 studies' / 'A total of 14 studies' / 'In total, 16 sets of results'), the headline MD mislabelled µmol/L when the pooled means are mg/dL, and acknowledged funnel asymmetry with 'a lack of studies showing null or negative effects.' The pooled GFR number appears only inside a figure; the CI still admits a ~5 mL/min decrement. |
| Longobardi, Gualano, Seguro, Roschel 2023 · Nutrients | observational | supports | low | Narrative review (self-declared; no search strategy, no risk-of-bias, no pooling) of case reports, animal studies and ~30 controlled human trials. Direction is stated outright: 'Despite some anecdotal reports and experimental data suggesting that creatine could be deleterious to the kidneys, cumulative evidence from independent, randomized controlled trials clearly show this is not the case.' It names the exact artifact this claim rests on - 'Creatine supplementation may increase serum creatinine (Crn) concentration for some individuals, but it does not necessarily indicate kidney dysfunction, as creatine is spontaneously converted into Crn' - and audits the case reports as confounded ('It is more likely that all these cases are related to abnormal exercise training regimens' plus steroid and multi-supplement use). Three limits the old extract dropped: the verdict is dose-conditioned ('creatine supplementation should be used in rational doses (up to 20 g/day)'); it explicitly does NOT extend to kidney disease ('There is also very limited evidence that creatine supplementation is safe for those with pre-existing kidney diseases, a very important limitation in the literature'; 'it is prudent to avoid creatine supplementation for those who have pre-existing kidney diseases resulting in very low kidney functions'); and 'there is a scant amount of long-term studies' beyond 16 weeks with accurate measures. Its quantitative anchor is one small meta-analysis it calls weak itself - 'Indeed, the low number of studies included in the meta-analysis weakens its conclusions' - and that meta-analysis is already in the vault as s31375416, so this review re-counts by construction. Stance stays supports; quality stays low, and it should: senior author Bruno Gualano 'has received research grants, creatine donation for scientific studies, travel support ... and honorarium for speaking at lectures from AlzChem (a company which manufactures creatine). Additionally, he serves as a member of the Scientific Advisory Board for Alzchem', which the funding line ('This research received no external funding') does not cover, and much of the human evidence narrated is the authors' own ('Our laboratory carried out several studies ...'). |
| de Souza e Silva 2019 · J Renal Nutr | meta-analysis | mixed | low | SR+MA, 6 of 15 studies pooled. The paper concludes 'creatine supplementation does not induce renal damage in the studied amounts and durations', but its own numbers say otherwise: serum creatinine SMD = 0.48 (95% CI 0.24-0.73, P = .001, I2 = 22%) and plasma urea SMD = 1.10 (95% CI 0.34-1.85, P = .004, I2 = 28%) - both CIs exclude zero, yet both are described as 'did not significantly alter'. Prose and statistics point opposite ways, so no clean sign; tempered to mixed. Only creatinine and urea measured - no GFR, cystatin C or albuminuria - so artifact vs harm is untestable here, and the abstract never states the pooled populations were healthy. Total n not reported. |
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