Evidence reference only. Not medical advice, not a dosing guide, and not a recommendation to use any drug.
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renal

22 findings across 10 drug records. Domain pages are descriptive indexes, not advice.

The grade rates how strong the evidence is, not how good or safe the drug is. A low or very-low grade means the evidence is thin, not that an effect is harmful or ruled out.

Most represented records

Native glucagon physiology (5)

Dulaglutide (4)

Tirzepatide (3)

Cotadutide (2)

Native GIP infusion and GIP(3-30) antagonist probe (2)

Semaglutide (2)

Efpeglenatide (1)

Liraglutide (1)

Evidence spread

High evidence 2 Moderate evidence 12 Low evidence 8 Very low evidence 0

Cotadutide DISCONTINUED
renal Decrease
Moderate evidence

A PK/PD model from the same phase 2b CKD/T2D study predicted ~-45.6% UACR and ~-47.2% urinary-albumin change versus placebo at 26 weeks with 600 ug cotadutide,...

Yu et al., Br J Clin Pharmacol 2025;91(9):2672-2683 Source
Full findingA PK/PD model from the same phase 2b CKD/T2D study predicted ~-45.6% UACR and ~-47.2% urinary-albumin change versus placebo at 26 weeks with 600 ug cotadutide, corroborating the dose-dependent antialbuminuric effect.
PopulationSecondary PK/PD modelling analysis of the phase 2 randomised controlled trial NCT04515849 (247 participants); cotadutide 100/300/600 ug vs semaglutide 1 mg vs placebo.
Fundingindustry - AstraZeneca (cotadutide PK/PD analysis; disclosed)
Comparatorsplacebo; semaglutide 1 mg
Cotadutide DISCONTINUED
renal Decrease
Moderate evidence

In a phase 2b trial in T2D + CKD, cotadutide (GLP-1/glucagon dual agonist) dose-dependently reduced urinary albumin-to-creatinine ratio versus placebo, reaching...

Selvarajah V et al., Kidney Int 2024;106(6):1170-1180 Source
Full findingIn a phase 2b trial in T2D + CKD, cotadutide (GLP-1/glucagon dual agonist) dose-dependently reduced urinary albumin-to-creatinine ratio versus placebo, reaching significance at 300 ug (-43.9%) and 600 ug (-49.9%) at week 14, sustained to week 26, on top of standard of care.
PopulationPhase 2 double-blind randomised controlled trial (NCT04515849): 248 randomised; T2D + CKD (eGFR 20 to <90, UACR >50 mg/g); cotadutide 100/300/600 ug daily vs placebo, vs open-label semaglutide 1 mg.
Fundingindustry - AstraZeneca (cotadutide phase 2b sponsor; disclosed)
Comparatorsplacebo; semaglutide 1 mg
Dulaglutide MARKETED
renal Decrease
Moderate evidence

REWIND exploratory renal composite reduced with dulaglutide versus placebo (albuminuria-driven; eGFR-decline/RRT components non-significant).

Gerstein HC et al. (REWIND renal), Lancet, 2019;394:131-138 Source
PopulationREWIND: N=9,901 T2D; median 5.4 years; exploratory analysis.
Fundingindustry - Eli Lilly and Company
Comparatorsplacebo
Dulaglutide MARKETED
renal Decrease
Moderate evidence

AWARD-7: dulaglutide slowed eGFR decline and reduced UACR versus insulin glargine at 52 weeks in T2D with moderate-to-severe CKD (parent-trial primary finding; the...

Am J Nephrol, 2023 (AWARD-7 fibrosis biomarkers) Source
Full findingAWARD-7: dulaglutide slowed eGFR decline and reduced UACR versus insulin glargine at 52 weeks in T2D with moderate-to-severe CKD (parent-trial primary finding; the captured paper reports fibrosis biomarkers).
PopulationAWARD-7 subset N=330 (dulaglutide 1.5 mg vs insulin glargine); T2D + moderate-to-severe CKD; 52 weeks; post hoc biomarker analysis.
Fundingindustry - Eli Lilly
Comparatorsinsulin glargine; dulaglutide 0.75 mg
Dulaglutide MARKETED
renal Decrease
Moderate evidence

AWARD-7 exploratory analysis: dulaglutide 1.5 mg reduced the composite of >=40% eGFR decline or ESKD versus insulin glargine in T2D with moderate-to-severe CKD,...

Tuttle KR et al. (AWARD-7 exploratory), Kidney360 2020;2(2):254-262 Source
Full findingAWARD-7 exploratory analysis: dulaglutide 1.5 mg reduced the composite of >=40% eGFR decline or ESKD versus insulin glargine in T2D with moderate-to-severe CKD, concentrated in the macroalbuminuria subgroup; benefit at MATCHED glycaemia and BP argues for a glycaemia-independent renal effect.
PopulationAWARD-7 prespecified exploratory secondary analysis of a randomised controlled trial: dulaglutide 0.75/1.5 mg weekly vs daily insulin glargine; T2D + moderate-to-severe CKD (stage 3-4); 1 year; active comparator at matched glycaemia/BP.
Fundingindustry - Eli Lilly and Company (AWARD-7 sponsor; disclosed)
Comparatorsinsulin glargine; dulaglutide 0.75 mg
Dulaglutide MARKETED
renal Mixed
Moderate evidence

AWARD-7 parent trial: in type 2 diabetes with moderate-to-severe CKD, dulaglutide gave HbA1c control non-inferior to insulin glargine with a slower decline in eGFR...

Tuttle KR, Lakshmanan MC, Rayner B, et al. Dulaglutide versus insulin glargine in patient... Source
Full findingAWARD-7 parent trial: in type 2 diabetes with moderate-to-severe CKD, dulaglutide gave HbA1c control non-inferior to insulin glargine with a slower decline in eGFR over 52 weeks.
PopulationAWARD-7: phase-3, multicentre, open-label, randomised trial, N=577; type 2 diabetes plus moderate-to-severe CKD (stages 3-4) on ACEi/ARB; dulaglutide 1.5/0.75 mg vs daily insulin glargine, both with insulin lispro; 52 weeks; NCT01621178.
Fundingindustry - Eli Lilly (trial sponsor; inferred from registration trial)
Comparatorsinsulin glargine
Efpeglenatide INVESTIGATIONAL
renal Decrease
Moderate evidence

AMPLITUDE-O: in T2D with cardiovascular disease or kidney disease plus a risk factor, efpeglenatide reduced a composite renal outcome (decreased kidney function or new...

Gerstein HC et al., N Engl J Med, 2021 Source
Full findingAMPLITUDE-O: in T2D with cardiovascular disease or kidney disease plus a risk factor, efpeglenatide reduced a composite renal outcome (decreased kidney function or new macroalbuminuria) versus placebo (HR 0.68), a prespecified secondary alongside the MACE primary.
PopulationAMPLITUDE-O (NCT03496298): 4076 randomised (2717 efpeglenatide 4/6 mg, 1359 placebo); T2D + CVD or CKD (eGFR 25.0-59.9) + a risk factor; median follow-up 1.81 years; double-blind RCT; SGLT2i-stratified.
Fundingindustry - Sanofi (efpeglenatide, AMPLITUDE-O; disclosed)
Comparatorsplacebo
Native GIP infusion and GIP(3-30) antagonist probe STATUS UNKNOWN
renal Not directional
Low evidence

No published study has measured a direct renal effect (natriuresis, sodium handling, GFR, renal blood flow) of selective/isolating GIP-receptor agonism, GIP infusion,...

Absence established via PubMed sweep (2026-06-21): no dual-agonist CV-outcome-trial recor... Source
Full findingNo published study has measured a direct renal effect (natriuresis, sodium handling, GFR, renal blood flow) of selective/isolating GIP-receptor agonism, GIP infusion, or GIPR antagonism in humans; renal GIP-receptor expression is sparse and the independent renal contribution of the GIP arm is unestablished. Honest gap record.
PopulationNarrative review (GIP in cardiovascular and kidney disease) attesting the absence/controversy; carries no positive attribution.
Fundingacademic / non-commercial (De Fano GIP review; no industry sponsor; disclosed)
Native GIP infusion and GIP(3-30) antagonist probe STATUS UNKNOWN
renal No change
Low evidence

An oral sodium-load study in 10 lean healthy men found that adding 6 g NaCl to an oral glucose load selectively amplified postprandial plasma GLP-1 but did NOT change...

Asmar A et al., Physiol Rep 2020;8(15):e14519 Source
Full findingAn oral sodium-load study in 10 lean healthy men found that adding 6 g NaCl to an oral glucose load selectively amplified postprandial plasma GLP-1 but did NOT change the postprandial GIP response; the proposed acute feed-forward natriuretic gut-kidney signal was attributed to GLP-1, with GIP showing no sodium-sensitivity.
Population10 lean healthy male participants; crossover (75 g glucose + 6 g NaCl vs glucose alone).
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Comparatorsglucose alone (no added NaCl)
Native GLP-1 physiology STATUS UNKNOWN
renal Increase
Low evidence

GLP-1 increases natriuresis principally by inhibiting the sodium-hydrogen exchanger isoform 3 (NHE3) in the renal proximal tubule, a candidate mechanism for the...

Skov J, Rev Endocr Metab Disord 2014;15(3):197-207 Source
Full findingGLP-1 increases natriuresis principally by inhibiting the sodium-hydrogen exchanger isoform 3 (NHE3) in the renal proximal tubule, a candidate mechanism for the antihypertensive effect of GLP-1 receptor agonists; GLP-1 regulation of GFR is more complex and may involve atrial natriuretic peptide and the renin-angiotensin system.
PopulationReview-tier mechanism synthesis of GLP-1 renal actions (human-relevant physiology).
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Native glucagon physiology STATUS UNKNOWN
renal Increase
Low evidence

Acute glucagon infusion raises renal plasma flow, GFR and natriuresis at the isolated GCGR level, whereas pure GLP-1R agonism is natriuretic but does not change...

Farah AE, Pharmacol Rev 1983;35(3):181-217 (Glucagon and the circulation) Source
Full findingAcute glucagon infusion raises renal plasma flow, GFR and natriuresis at the isolated GCGR level, whereas pure GLP-1R agonism is natriuretic but does not change GFR/RPF at healthy baseline; the co-agonist-minus-GLP-1 logic therefore attributes any GFR/RPF rise on a co-agonist toward the GCGR arm, with both arms independently natriuretic suggesting additive natriuresis.
PopulationReview-tier (glucagon side, Farah 1983); GLP-1 contrast poles are human-primary (Skov JCEM 2013 PMID 23463656; Asmar AJP-Endo 2015 PMID 25670826) cited as contrast only.
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Native glucagon physiology STATUS UNKNOWN
renal Increase
Low evidence

Starvation (fasting) natriuresis has been linked to raised circulating glucagon, the likely mechanism being that glucagon increases renal excretion of organic acids by...

Farah AE, Pharmacol Rev 1983;35(3):181-217 (Glucagon and the circulation) Source
Full findingStarvation (fasting) natriuresis has been linked to raised circulating glucagon, the likely mechanism being that glucagon increases renal excretion of organic acids by inhibiting their tubular reabsorption.
PopulationReview-tier synthesis; the fasting-natriuresis/glucagon link is correlational.
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Native glucagon physiology STATUS UNKNOWN
renal Increase
Low evidence

Glucagon increased RNA concentration in glomerular tissue (a cAMP-independent effect), related to glomerular enlargement and basement-membrane thickening seen in...

Farah AE, Pharmacol Rev 1983;35(3):181-217 (Glucagon and the circulation) Source
Full findingGlucagon increased RNA concentration in glomerular tissue (a cAMP-independent effect), related to glomerular enlargement and basement-membrane thickening seen in poorly controlled insulin-dependent diabetes (low insulin, high glucagon); the increased glomerular filtration of poorly controlled diabetes has been linked to the same hyperglucagonaemia.
PopulationReview-tier synthesis; chronic-hyperglucagonaemia/diabetes association data.
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Native glucagon physiology STATUS UNKNOWN
renal Increase
Low evidence

In 24 healthy young men, a 7-day high-protein versus normal-protein diet raised glomerular filtration rate by ~13% and filtration fraction, with concurrent rises in...

Frank H et al., Am J Clin Nutr 2009;90(6):1509-16 Source
Full findingIn 24 healthy young men, a 7-day high-protein versus normal-protein diet raised glomerular filtration rate by ~13% and filtration fraction, with concurrent rises in plasma GLUCAGON, natriuresis, urinary albumin and urea; renal plasma flow and renal vascular resistance were unchanged.
Population24 healthy young men; 7-day high-protein (2.4 g/kg/d) vs normal-protein (1.2 g/kg/d) crossover.
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Comparatorsnormal-protein diet
Native glucagon physiology STATUS UNKNOWN
renal Increase
Low evidence

At relatively large doses glucagon increased renal plasma flow, glomerular filtration and electrolyte excretion; intra-renal-arterial injection raised electrolyte...

Farah AE, Pharmacol Rev 1983;35(3):181-217 (Glucagon and the circulation) Source
Full findingAt relatively large doses glucagon increased renal plasma flow, glomerular filtration and electrolyte excretion; intra-renal-arterial injection raised electrolyte excretion on the injected side with minimal/no GFR change, indicating a DIRECT renal tubular natriuretic action probably mediated via tubular cAMP and prostaglandin formation in the ascending limb and collecting ducts.
PopulationReview-tier synthesis of glucagon renal physiology (mixed-species mechanism; gross RPF/GFR/excretion rise the human-relevant datum).
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Liraglutide MARKETED
renal Decrease
Moderate evidence

LEADER prespecified secondary renal composite reduced with liraglutide versus placebo (driven by new macroalbuminuria).

Mann JFE et al. (LEADER renal), NEJM, 2017;377:839-848 Source
PopulationLEADER: N=9,340 T2D, high CV risk; median 3.84 years; RCT.
Fundingindustry-Novo Nordisk + academic-NIH (co-funded)
Comparatorsplacebo
Retatrutide INVESTIGATIONAL
renal Mixed
Moderate evidence

Pooled post hoc of two phase 2 trials: higher-dose retatrutide reduced UACR in T2D and obesity, and increased eGFR in obesity but not in T2D.

Heerspink HJL et al. (retatrutide kidney), Kidney Int Rep, 2025;10:1980-1992 Source
PopulationPooled post hoc, 2 phase 2 RCTs; T2D n=281 (wk36, dula comparator) and obesity n=338 (wk48); eGFR >=45.
Fundingindustry-Eli Lilly
Comparatorsplacebo; dulaglutide 1.5 mg (T2D study)
Semaglutide MARKETED
renal Decrease
High evidence

FLOW: in T2D + CKD, semaglutide reduced the primary composite kidney outcome versus placebo; trial stopped early for efficacy. eGFR slope also less steep.

Perkovic V et al. (FLOW), NEJM, 2024 Source
PopulationFLOW: N=3,533 T2D + CKD; median follow-up 3.4 years; double-blind RCT vs placebo.
Fundingindustry - Novo Nordisk (disclosed in publication)
Comparatorsplacebo
Semaglutide MARKETED
renal Decrease
High evidence

SUSTAIN-6 prespecified secondary: lower rate of new or worsening nephropathy with semaglutide versus placebo.

Marso SP et al. (SUSTAIN-6), NEJM, 2016 Source
PopulationSUSTAIN-6: N=3,297 T2D; 104 weeks; RCT.
Fundingindustry - Novo Nordisk
Comparatorsplacebo
Tirzepatide MARKETED
renal Decrease
Moderate evidence

SURPASS-4 post hoc: tirzepatide slowed eGFR decline, prevented UACR rise and reduced a composite kidney endpoint versus insulin glargine.

Heerspink HJL et al. (SURPASS-4 kidney), Lancet Diabetes Endocrinol, 2022;10:774-785; cys... Source
PopulationSURPASS-4: N=1,995 (995 tirz, 1000 glargine); T2D, high CV risk; median treatment 85 weeks; open-label; post hoc.
Fundingindustry-Eli Lilly
Comparatorsinsulin glargine
Tirzepatide MARKETED
renal Decrease
Moderate evidence

SURPASS-CVOT prespecified exploratory: tirzepatide reduced major kidney events versus dulaglutide (direct incretin head-to-head).

Zoungas S et al. Tirzepatide vs dulaglutide on major kidney events: pre-specified explora... Source
PopulationSURPASS-CVOT: N=13,299 (6586 tirz, 6579 dula; 2948 high-risk CKD); T2D + ASCVD; median 4.0 years; double-blind.
Fundingindustry-Eli Lilly
Comparatorsdulaglutide 1.5 mg
Tirzepatide MARKETED
renal Decrease
Moderate evidence

In T2D with established ASCVD, tirzepatide reduced a composite of major adverse kidney events versus dulaglutide in a prespecified exploratory analysis of...

Zoungas S et al. Tirzepatide vs dulaglutide on major kidney events: pre-specified explora... Source
Full findingIn T2D with established ASCVD, tirzepatide reduced a composite of major adverse kidney events versus dulaglutide in a prespecified exploratory analysis of SURPASS-CVOT. Note the comparator is an active CV-proven GLP-1RA (dulaglutide), NOT placebo, and the analysis is exploratory (not part of the confirmatory hierarchy).
PopulationPrespecified exploratory analysis of SURPASS-CVOT (NCT04255433): n=13,165 with T2D + established ASCVD; tirzepatide (max-tolerated up to 15 mg) vs dulaglutide 1.5 mg; median follow-up 4.0 years.
Fundingindustry-Eli Lilly
Comparatorsdulaglutide 1.5 mg