# Do GLP-1 Drugs Prevent Contrast Kidney Injury? 8.7% Against 25.7% | This GLP Do GLP-1 drugs prevent contrast-induced kidney injury? In 336 adults having coronary angiography it was 8.7% against 25.7%, odds ratio 0.290 | creatinine did not differ. Publisher: This GLP Editorial Team Canonical: https://thisglp.com/research/do-glp1-drugs-prevent-contrast-kidney-injury Updated: 2026-09-18 Published: 2026-09-17 [← Research](https://thisglp.com/research) Evidence # Do GLP-1 Drugs Prevent Contrast Kidney Injury? 8.7% Against 25.7% One retrospective cohort found a third the rate of kidney injury after coronary angiography. The outcome is defined by a creatinine rise, and creatinine itself came out at p = 0.084. [This GLP Editorial Team](https://thisglp.com/about)September 20268 min read Two readings of the same kidneys, 48 to 72 hours after contrast · The event, defined as a creatinine rise · 8.7% on a GLP-1 · 25.7% not · odds ratio 0.290, 95% CI 0.119 to 0.708 · The creatinine the definition rests on · 1.02 mg/dL against 1.17 — p = 0.084, not significant. · eGFR, which is calculated from creatinine, did differ: · 67.1 against 58.0 mL/min/1.73 m², p < 0.001. **Research, not medical advice.** This GLP is independent and educational. Nothing here is a substitute for individualized care from a licensed clinician, and reading it creates no doctor–patient relationship. Talk to your own provider before starting, stopping, or changing any medication, peptide, or therapy. See our [methodology](https://thisglp.com/methodology) and [terms](https://thisglp.com/terms). In one retrospective cohort, yes. Contrast-induced kidney injury occurred in 8.7% of GLP-1 users against 25.7% of non-users [\[1\]](https://thisglp.com/research/do-glp1-drugs-prevent-contrast-kidney-injury#ref-1). The adjusted odds ratio was 0.290, 95% CI 0.119 to 0.708. That outcome is defined by a creatinine rise. Creatinine itself did not differ significantly, at p = 0.084. Nobody was randomized, and the cohort is 336 people at one center. ## Key takeaways - 336 adults with type 2 diabetes undergoing coronary angiography or PCI at one center. - 149 were on a GLP-1 drug and 187 were not. Nobody was randomized or matched. - Contrast-induced kidney injury occurred in 8.7% against 25.7%, odds ratio 0.290, 95% CI 0.119 to 0.708. - That outcome is defined by a creatinine rise, and creatinine itself did not differ significantly (p = 0.084). - eGFR, which is calculated from creatinine, did differ: 67.1 against 58.0. A kidney injury here is not something anybody felt. It is a definition: creatinine up by at least 0.5 mg/dL, or by at least a quarter, within seventy-two hours. Hold that next to the fact that creatinine did not differ significantly between the two groups. The randomized kidney evidence for this drug class is a separate body of work, summarized in [the FLOW trial](https://thisglp.com/research/semaglutide-and-kidney-disease). ## Both numbers, side by side The event rate was 8.7% among GLP-1 users and 25.7% among non-users. Adjusted, the odds ratio came to 0.290 with an interval of 0.119 to 0.708. At the same timepoint, mean creatinine was 1.02 mg/dL in users and 1.17 in non-users, p = 0.084. Those standard deviations are wide, at 0.73 and 1.57. A difference in group means can be absent while a difference in how many people cross a threshold is large. That is not a contradiction and it is not nothing either. A threshold outcome and a mean are different questions about the same measurement. A paper reporting both has told you something a paper reporting only the first would not. That is how [a ratio and an absolute risk](https://thisglp.com/research/bigger-relative-smaller-absolute) describe one finding in two sizes. eGFR is calculated, not measured Estimated GFR is derived from creatinine, age and sex. It came out 67.1 against 58.0 with p below 0.001, while the creatinine it is built from sat at p = 0.084. Some of that is baseline: if the groups differed in kidney function before the procedure, the calculation carries the difference forward. The rest is what an equation built on muscle metabolism does when the people being compared differ in body composition, which on these drugs they reliably do. That last point is not theoretical. A propensity-matched study of semaglutide in polycystic kidney disease used eGFR as its outcome [\[2\]](https://thisglp.com/research/do-glp1-drugs-prevent-contrast-kidney-injury#ref-2). The same dependency applies wherever a drug changes lean mass. The fuller reading of that trap is in [the eGFR and muscle problem](https://thisglp.com/research/can-you-take-a-glp1-with-polycystic-kidney-disease). ## What the design can carry 336 people at one center, looked at afterwards. Users were compared with non-users by regression rather than by matching. Nobody chose who got what. An odds ratio of 0.29 is a large effect. Large effects from small retrospective cohorts are the ones that most often shrink when somebody randomizes. The usual reason is that the two groups differed in ways nobody recorded. [A hazard ratio its own authors distrust](https://thisglp.com/research/glp1-mortality-authors-doubt-their-own) shows that at the extreme. ## What the randomized evidence says about kidneys The strongest kidney result for this drug class comes from a trial that stopped early. FLOW randomized people with type 2 diabetes and chronic kidney disease to semaglutide or placebo [\[3\]](https://thisglp.com/research/do-glp1-drugs-prevent-contrast-kidney-injury#ref-3). It was halted for efficacy on a composite of kidney failure, sustained eGFR decline and death. That is chronic disease progression over years, not a creatinine spike in seventy-two hours. The two questions are related and they are not the same. Nothing in the chronic evidence predicts what happens around a scheduled dose of contrast dye. Nothing in a 336-person cohort establishes it either. ## Why it is still worth reading Contrast injury is common, it is expensive, and it happens on a schedule somebody controls. A drug patients are already taking that reduced it would matter. There is a plausible route: better volume status, less inflammation, improved endothelial function. So this is a hypothesis with a mechanism, measured in a way that leaves room for doubt. The useful next step is a trial that randomizes around a scheduled procedure. Nothing here is a reason to start, stop or time a dose around an angiogram. Tell the team doing the procedure what you take and let them decide. ## Frequently asked Do GLP-1 drugs prevent contrast-induced kidney injury? One retrospective cohort of 336 adults found 8.7% against 25.7%, an adjusted odds ratio of 0.290. Nobody was randomized, and the creatinine measurement the outcome is built from did not differ significantly. Why does the creatinine result matter? Contrast-induced kidney injury is defined as a creatinine rise of at least 0.5 mg/dL or 25% within 72 hours. Mean creatinine came out at p = 0.084, so the threshold count moved while the underlying measurement did not separate. Should a dose be timed around an angiogram? Nothing here supports starting, stopping or timing a dose around a procedure. Tell the team doing the procedure what you take. What do the randomized kidney trials show? FLOW randomized people with type 2 diabetes and chronic kidney disease to semaglutide or placebo and was stopped early for efficacy on a composite of kidney failure, sustained eGFR decline and death. That is disease progression over years, not a creatinine spike in 72 hours. ## Sources 1. \[1\] Oksen D, et al. (2026). Effects of GLP-1 receptor agonists on the incidence of contrast-induced acute kidney injury in patients with Type 2 diabetes mellitus undergoing coronary interventions Frontiers in Endocrinology. [PMID 42723898](https://pubmed.ncbi.nlm.nih.gov/42723898/) 2. \[2\] Chen TP, et al. (2026). Association of semaglutide use with kidney outcomes in adults with ADPKD: A propensity score-matched real-world study Science Progress. [PMID 42648283](https://pubmed.ncbi.nlm.nih.gov/42648283/) 3. \[3\] Perkovic V, et al. (2024). Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes The New England Journal of Medicine. 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