GLP-1 Evidence

Not medical advice. A record of published research and our assessments of it. The limits

Effects of GLP-1 receptor agonists on kidney and cardiovascular disease outcomes: a meta-analysis of randomised controlled trials

Design
Meta-analysis · 85373 participants · Hard outcome
Match to healthy normal-weight adults aged 55–75
Different populationDiabetes trials plus SELECT; no heterogeneity between SELECT and the diabetes trials, which modestly extends the finding to obesity without diabetes.
Could weight loss explain it?
Possibly[Auto] Not addressed in abstract.
Study tier
Study tier 1Meta-analysis of large randomized trials with hard kidney outcomes.
Assessment
Version 2 · curated · Sep 13, 2026

Study facts come from the paper. Population match, weight-loss explanation and study tier are our judgments, made against the reference group of healthy normal-weight adults aged 55–75.

Across 11 randomized trials (85,373 people, mostly with type 2 diabetes), GLP-1 receptor agonists reduced kidney failure by 16% and a composite kidney outcome by 18%, with consistent results when SELECT was added. No increase in serious adverse events or pancreatitis.

01Findings

What the study reported

Drugs
Class unspecified, Semaglutide, Liraglutide, Dulaglutide, Exenatide, Efpeglenatide
Comparator
placebo
Primary outcome
Composite kidney outcome (kidney failure, sustained >=50% eGFR loss, kidney death) and MACE across 11 RCTs
Effect
Kidney composite HR 0.82; kidney failure HR 0.84; MACE HR 0.87; all-cause death HR 0.88 (T2D); similar including SELECT
95% confidence interval
0.73 to 0.93 (kidney composite)
Follow-up
12 months of follow-up
Adverse events
Not extracted
Limitations
Auto-classified from abstract only; effect estimates, adverse events and limitations not extracted. Requires manual review.

Who was studied

Bmi mean
27
Bmi min
27
Diabetes status
type 2 diabetes in 10 trials; SELECT (no diabetes, obesity) added post hoc
Cvd status
cardiovascular disease present in population (see abstract)
Sample size
500

Study quality details

Study design
Meta-analysis
Sample size
500
Randomization
n/a
Blinding
not stated
Comparator
placebo
Follow up duration
12 months of follow-up
Outcome type
mixed
Replication
11 trials; low heterogeneity for kidney failure
Consistency with other evidence
not assessed (auto)
Population applicability
UNKNOWN
Statistical precision
CI reported: 95% CI 0·73-0·93
Risk of bias
trial-level; SELECT added post hoc
Funding conflicts
unclear
Peer review status
yes
02Funding

Funding and conflicts

Funding
Not stated in abstract
Industry funded
Unclear
Manufacturer
Novo Nordisk, Eli Lilly, Lilly, AstraZeneca, Sanofi, Boehringer Ingelheim, Amgen, Pfizer, Roche, Hanmi
Sponsor role
not reported in abstract
Author conflicts
Authors report consulting/speaking fees from Bayer, AstraZeneca, Novo Nordisk and others.
Independent replication
yes (consistent with PMID 34425083)

Funding is shown on every study and never used to score it.

03Claims

Claims this study bears on

04Source

The source, as retrieved

Abstract

[BACKGROUND] GLP-1 receptor agonists reduce the risk of major adverse cardiovascular events (MACE) and can also have kidney benefits. However, whether GLP-1 receptor agonists improve clinically important kidney outcomes remains uncertain. We aimed to comprehensively assess the effects of GLP-1 receptor agonists on kidney and cardiovascular disease outcomes by performing a meta-analysis of randomised controlled trials. [METHODS] For this meta-analysis, we searched MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials for randomised controlled trials that included at least 500 participants with type 2 diabetes, compared a GLP-1 receptor agonist with placebo with at least 12 months of follow-up, and reported a primary clinical kidney or cardiovascular outcome, from database inception to March 26, 2024. Post hoc, we included the SELECT trial (NCT03574597), which enrolled participants with cardiovascular disease and a BMI of 27 kg/m2 or more without diabetes. Study-level summary data were extracted independently by two authors for inclusion in this random-effects analysis. The main kidney outcome was a composite outcome, consisting of kidney failure (kidney replacement therapy or a persistent estimated glomerular filtration rate [eGFR] <15 mL/min per 1·73 m2), a sustained reduction in eGFR by at least 50% or the nearest equivalent, or death from kidney failure. The main cardiovascular outcome was MACE, consisting of cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke. This study is registered with PROSPERO, CRD42024528864. [FINDINGS] Of the 5140 records identified through the literature search, 11 trials, involving 85 373 participants (29 386 female, 55 987 male), were included in the meta-analysis. In participants with type 2 diabetes (67 769), GLP-1 receptor agonists reduced the composite kidney outcome by 18% compared with placebo (hazard ratio [HR] 0·82, 95% CI 0·73-0·93; I2 =26·41%), kidney failure by 16% (HR 0·84, 0·72-0·99; I2 =0%), MACE by 13% (HR 0·87, 0·81-0·93; I2 =49·75%), and all-cause death by 12% (HR 0·88, 0·83-0·93; I2 =0%). The effect on the composite kidney outcome (HR 0·81, 95% CI 0·72-0·92; I2 =23·11%), kidney failure (HR 0·84, 0·72-0·98; I2 =0%), MACE (HR 0·86, 0·80-0·92; I2 =48·9%), and all-cause death (HR 0·87, 0·82-0·91; I2 =0%) was similar when the SELECT trial was included, with no evidence of heterogeneity between this trial and those including participants with type 2 diabetes (pheterogeneity >0·05). There was no difference in the risk of serious adverse events, including acute pancreatitis and severe hypoglycaemia, between the GLP-1 receptor agonist and placebo groups (risk ratio [RR] 0·95, 95% CI 0·90-1·01; I2 =88·5%). However, treatment discontinuation due to adverse events occurred more frequently in the GLP-1 receptor agonist groups (RR 1·51, 95% CI 1·18-1·94; I2 =96·3%). [INTERPRETATION] We found evidence that GLP-1 receptor agonists significantly reduce clinically important kidney events, kidney failure, and cardiovascular events. [FUNDING] None.

Where this record came from

SourceRetrievedIdentifier
pubmedSep 13, 202639608381
first ingestion