---
title: "Semaglutide preserves kidney function in type 2 diabetes: mechanisms from the REMODEL randomized t"
id: "nature-1-effects-of-semaglutide-on-kidney-disease-in-type-2-diabetes-a-randomized"
canonical_url: "https://medichelpline.com/clinical-feed/nature-1-effects-of-semaglutide-on-kidney-disease-in-type-2-diabetes-a-randomized"
content_type: "clinical_feed_article"
specialty: "Nephrology"
source_name: "Nature Medicine"
source_url: "https://www.nature.com/articles/s41591-026-04674-2"
published_at: "2026-10-01T10:49:30.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Semaglutide preserves kidney function in type 2 diabetes: mechanisms from the REMODEL randomized t
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/nature-1-effects-of-semaglutide-on-kidney-disease-in-type-2-diabetes-a-randomized
- **Specialty:** [Nephrology](https://medichelpline.com/clinical-feed/nephrology.md)
- **Primary Source:** Nature Medicine
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41591-026-04674-2)
- **Published At:** 2026-10-01T10:49:30.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The REMODEL trial investigated kidney-specific mechanisms of the GLP-1 receptor agonist **semaglutide** in people with type 2 diabetes (T2D) and chronic kidney disease (CKD) using imaging, histology and transcriptomics over 52 weeks. 106 participants were randomized (71 semaglutide, 35 placebo). 33 participants underwent paired kidney biopsies and 22 had single-nucleus RNA sequencing; 13 had spatial transcriptomics. - Coprimary kidney magnetic resonance imaging (MRI) endpoints—renal oxygenation (R2*), global perfusion and tissue inflammation (T1 mapping)—showed no significant differences between semaglutide and placebo after 52 weeks. - Secondary imaging and physiological outcomes indicated a significant reduction in **renal artery resistive index** with semaglutide and stabilization of the apparent diffusion coefficient (ADC), interpreted as prevention of fibrosis progression. - Molecular profiling demonstrated pronounced effects of semaglutide on **glomerular endothelial cells**, and spatial analyses showed fewer immune cells in close proximity to these endothelial cells after treatment. - The findings point to putative kidney-protective mechanisms for semaglutide that include reduced vascular resistance, attenuation of fibrotic progression and improved endothelial cell–related molecular programs. - REMODEL complements clinical outcome data from the FLOW trial, which showed a 24% reduction in risk of a composite kidney outcome with semaglutide in a similar population. - Baseline trial population: mean age 65.3 years, 23.6% women, mean eGFRcreatinine 51.1 ml min−1 per 1.73 m2, median UACR 187.3 mg g−1, mean HbA1c 7.1%. Nearly all participants were on renin–angiotensin system inhibitors; 39.6% used SGLT2 inhibitors overall and 54.5% among the biopsy subgroup. - ClinicalTrials.gov identifier: NCT04865770. Details on some exploratory measures, full statistical values and additional subgroup analyses were reported in the source article.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [nature medicine](https://www.nature.com/nm) 3. [articles](https://www.nature.com/nm/articles?type=article) 4. article Effects of semaglutide on kidney disease in type 2 diabetes: a randomized placebo-controlled trial [ Download PDF ](https://www.nature.com/articles/s41591-026-04674-2.pdf) [ Download PDF ](https://www.nature.com/articles/s41591-026-04674-2.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 01 October 2026 # Effects of semaglutide on kidney disease in type 2 diabetes: a randomized placebo-controlled trial * [Katherine R. Tuttle](https://www.nature.com/articles/s41591-026-04674-2#auth-Katherine_R_-Tuttle-Aff1-Aff2) [ORCID: orcid.org/0000-0002-2235-0103](https://orcid.org/0000-0002-2235-0103)[1](https://www.nature.com/articles/s41591-026-04674-2#Aff1),[2](https://www.nature.com/articles/s41591-026-04674-2#Aff2) [na1](https://www.nature.com/articles/s41591-026-04674-2#na1), * [Petter Bjornstad](https://www.nature.com/articles/s41591-026-04674-2#auth-Petter-Bjornstad-Aff3-Aff4) [ORCID: orcid.org/0000-0002-5160-2947](https://orcid.org/0000-0002-5160-2947)[3](https://www.nature.com/articles/s41591-026-04674-2#Aff3),[4](https://www.nature.com/articles/s41591-026-04674-2#Aff4) [na1](https://www.nature.com/articles/s41591-026-04674-2#na1), * [Cathy Smith](https://www.nature.com/articles/s41591-026-04674-2#auth-Cathy-Smith-Aff5) [ORCID: orcid.org/0000-0003-1518-9320](https://orcid.org/0000-0003-1518-9320)[5](https://www.nature.com/articles/s41591-026-04674-2#Aff5), * [Menno Pruijm](https://www.nature.com/articles/s41591-026-04674-2#auth-Menno-Pruijm-Aff6) [ORCID: orcid.org/0000-0003-1027-1851](https://orcid.org/0000-0003-1027-1851)[6](https://www.nature.com/articles/s41591-026-04674-2#Aff6), * [Phillip J. McCown](https://www.nature.com/articles/s41591-026-04674-2#auth-Phillip_J_-McCown-Aff5) [ORCID: orcid.org/0000-0002-8012-1931](https://orcid.org/0000-0002-8012-1931)[5](https://www.nature.com/articles/s41591-026-04674-2#Aff5), * [Jeffrey B. Hodgin](https://www.nature.com/articles/s41591-026-04674-2#auth-Jeffrey_B_-Hodgin-Aff7)[7](https://www.nature.com/articles/s41591-026-04674-2#Aff7), * [David Z. I. Cherney](https://www.nature.com/articles/s41591-026-04674-2#auth-David_Z__I_-Cherney-Aff8) [ORCID: orcid.org/0000-0003-4164-0429](https://orcid.org/0000-0003-4164-0429)[8](https://www.nature.com/articles/s41591-026-04674-2#Aff8), * [Nicolas Belmar](https://www.nature.com/articles/s41591-026-04674-2#auth-Nicolas-Belmar-Aff9)[9](https://www.nature.com/articles/s41591-026-04674-2#Aff9), * [Milenta Mariam Chacko](https://www.nature.com/articles/s41591-026-04674-2#auth-Milenta_Mariam-Chacko-Aff10) [ORCID: orcid.org/0009-0006-1465-2095](https://orcid.org/0009-0006-1465-2095)[10](https://www.nature.com/articles/s41591-026-04674-2#Aff10), * [Vivek Das](https://www.nature.com/articles/s41591-026-04674-2#auth-Vivek-Das-Aff9) [ORCID: orcid.org/0000-0003-0614-0373](https://orcid.org/0000-0003-0614-0373)[9](https://www.nature.com/articles/s41591-026-04674-2#Aff9), * [Thomas P. Gunnarsson](https://www.nature.com/articles/s41591-026-04674-2#auth-Thomas_P_-Gunnarsson-Aff9)[9](https://www.nature.com/articles/s41591-026-04674-2#Aff9), * [Thomas Idorn](https://www.nature.com/articles/s41591-026-04674-2#auth-Thomas-Idorn-Aff9) [ORCID: orcid.org/0009-0009-4896-5868](https://orcid.org/0009-0009-4896-5868)[9](https://www.nature.com/articles/s41591-026-04674-2#Aff9), * [Philip A. Schytz](https://www.nature.com/articles/s41591-026-04674-2#auth-Philip_A_-Schytz-Aff9)[9](https://www.nature.com/articles/s41591-026-04674-2#Aff9), * [Amaya Zaratiegui](https://www.nature.com/articles/s41591-026-04674-2#auth-Amaya-Zaratiegui-Aff9) [ORCID: orcid.org/0009-0007-6522-2703](https://orcid.org/0009-0007-6522-2703)[9](https://www.nature.com/articles/s41591-026-04674-2#Aff9) & * … * [Matthias Kretzler](https://www.nature.com/articles/s41591-026-04674-2#auth-Matthias-Kretzler-Aff5) [ORCID: orcid.org/0000-0003-4064-0582](https://orcid.org/0000-0003-4064-0582)[5](https://www.nature.com/articles/s41591-026-04674-2#Aff5) Show authors [_Nature Medicine_](https://www.nature.com/nm) (2026) [Cite this article](https://www.nature.com/articles/s41591-026-04674-2#citeas) [ Save article ](https://www.nature.com/articles/s41591-026-04674-2/save-research?_csrf=5edO4swvbkVOywIMDoKQNx-y4gBfTobU) [ View saved research ](https://www.nature.com/saved-research) ## Abstract The GLP-1 receptor agonist semaglutide preserves kidney function in people with type 2 diabetes and chronic kidney disease, but the underlying mechanisms are unclear. Here we report a 52-week randomized trial of subcutaneous semaglutide 1 mg once weekly versus placebo (_n_ = 106 (_n_ = 25 women, _n_ = 81 men)) in participants with type 2 diabetes and chronic kidney disease. To identify kidney-specific mechanisms of action for semaglutide, we performed integrated multiparametric magnetic resonance imaging of the kidney and biopsy for histology (_n_ = 33), alongside single-nucleus (_n_ = 22) and spatial transcriptomics (_n_ = 13) on paired samples with before- and after-treatment measurements. Coprimary magnetic resonance imaging outcomes (oxygenation by R2*, global perfusion and tissue inflammation by T1 mapping) were not significantly altered by semaglutide versus placebo treatment. Secondary outcomes revealed that semaglutide treatment, as compared to placebo, was associated with a significantly reduced renal artery resistive index and stabilization of the apparent diffusion coefficient, indicating prevention of fibrosis progression. Moreover, secondary transcriptomic outcomes revealed pronounced effects of semaglutide on glomerular endothelial cells, consistent with the results of spatial analyses indicating reduced numbers of immune cells in the proximity of these endothelial cells. The results from this trial indicate that mechanisms of kidney protection by semaglutide may include reduced vascular resistance, prevention of fibrosis and improved underlying molecular programs promoting endothelial cell health. ClinicalTrials.gov identifier: [NCT04865770](https://clinicaltrials.gov/study/NCT04865770). ### Explore related subjects Discover the latest articles and news in related subjects. * [Chronic kidney disease](https://www.nature.com/subjects/chronic-kidney-disease) * [Outcomes research](https://www.nature.com/subjects/outcomes-research) * [Incretin-Based Therapeutics for Type 2 Diabetes Management](https://www.nature.com/subjects/incretin-based-therapeutics-for-type-2-diabetes-management) ## Main Chronic kidney disease (CKD) affects nearly 800 million people and develops in 40% of those living with type 2 diabetes (T2D), making diabetes the leading cause of kidney failure worldwide[1](https://www.nature.com/articles/s41591-026-04674-2#ref-CR1 "Alicic, R. Z., Rooney, M. T. & Tuttle, K. R. Diabetic kidney disease: challenges, progress, and possibilities. Clin. J. Am. Soc. Nephrol. 12, 2032–2045 \(2017\)."),[2](https://www.nature.com/articles/s41591-026-04674-2#ref-CR2 "Tuttle, K. R. et al. Incidence of chronic kidney disease among adults with diabetes, 2015–2020. N. Engl. J. Med. 387, 1430–1431 \(2022\)."),[3](https://www.nature.com/articles/s41591-026-04674-2#ref-CR3 "Kovesdy, C. P. Epidemiology of chronic kidney disease: an update 2022. Kidney Int. Suppl. \(2011\) 12, 7–11 \(2011\)."),[4](https://www.nature.com/articles/s41591-026-04674-2#ref-CR4 "Collaborators, G. C. K. D. Global, regional, and national burden of chronic kidney disease in adults, 1990–2023, and its attributable risk factors: a systematic analysis for the Global Burden of Disease Study 2023. Lancet 406, 2461–2482 \(2025\)."). In the FLOW (evaluate renal Function with semagLutide Once Weekly) trial, subcutaneous semaglutide 1.0 mg once weekly reduced risk of the primary kidney outcome, defined as ≥50% decline in the estimated glomerular filtration rate (eGFR), kidney failure or death due to kidney or cardiovascular causes, by 24% in participants with T2D and CKD[5](https://www.nature.com/articles/s41591-026-04674-2#ref-CR5 "Perkovic, V. et al. Effects of semaglutide on chronic kidney disease in patients with type 2 diabetes. N. Engl. J. Med. 391, 109–121 \(2024\)."). Mechanisms for the kidney-protective effects of semaglutide are unclear. Mediation analyses from clinical trials of glucagon-like peptide (GLP-1) receptor agonists, including semaglutide, indicate that lowering of glycemia and body weight only partly explain the kidney benefit[6](https://www.nature.com/articles/s41591-026-04674-2#ref-CR6 "Colhoun, H. M. et al. Long-term kidney outcomes of semaglutide in obesity and cardiovascular disease in the SELECT trial. Nat. Med. 30, 2058–2066 \(2024\)."),[7](https://www.nature.com/articles/s41591-026-04674-2#ref-CR7 "Mann, J. F. E. et al. Potential kidney protection with liraglutide and semaglutide: Exploratory mediation analysis. Diab. Obes. Metab. 23, 2058–2066 \(2021\)."). Trials of dulaglutide and tirzepatide in people living with T2D showed no correlation between weight loss and eGFR, whether calculated with serum creatinine or cystatin C[8](https://www.nature.com/articles/s41591-026-04674-2#ref-CR8 "Heerspink, H. J. L. et al. Effects of tirzepatide versus insulin glargine on cystatin C-based kidney function: a SURPASS-4 post hoc analysis. Diab. Care 46, 1501–1506 \(2023\)."),[9](https://www.nature.com/articles/s41591-026-04674-2#ref-CR9 "Tuttle, K. R. et al. Body weight and eGFR during dulaglutide treatment in type 2 diabetes and moderate-to-severe chronic kidney disease \(AWARD-7\). Diab. Obes. Metab. 21, 1493–1497 \(2019\)."). GLP-1 receptors have been identified in the preglomerular vascular compartment, efferent arterioles, interlobular arteries and arcuate artery smooth muscle cells of human, monkey and rodent kidneys[10](https://www.nature.com/articles/s41591-026-04674-2#ref-CR10 "Hviid, A. V. R. & Sørensen, C. M. Glucagon-like peptide-1 receptors in the kidney: impact on renal autoregulation. Am. J. Physiol. Ren. Physiol. 318, F443–F454 \(2020\)."),[11](https://www.nature.com/articles/s41591-026-04674-2#ref-CR11 "Pyke, C. et al. GLP-1 receptor localization in monkey and human tissue: novel distribution revealed with extensively validated monoclonal antibody. Endocrinology 155, 1280–1290 \(2014\)."). In preclinical models, GLP-1 receptor agonists have shown a number of favorable effects on the kidney, including reduced inflammation and fibrosis along with increased GFR and decreased albuminuria[12](https://www.nature.com/articles/s41591-026-04674-2#ref-CR12 "Sourris, K. C. et al. Glucagon-like peptide-1 receptor signaling modifies the extent of diabetic kidney disease through dampening the receptor for advanced glycation end products-induced inflammation. Kidney Int. 105, 132–149 \(2024\)."),[13](https://www.nature.com/articles/s41591-026-04674-2#ref-CR13 "Ougaard, M. E. et al. Liraglutide improves the kidney function in a murine model of chronic kidney disease. Nephron 144, 595–606 \(2020\)."),[14](https://www.nature.com/articles/s41591-026-04674-2#ref-CR14 "Bjørnholm, K. D., Ougaard, M. E., Skovsted, G. F., Knudsen, L. B. & Pyke, C. Activation of the renal GLP-1R leads to expression of Ren1 in the renal vascular tree. Endocrinol. Diab. Metab. 4, e00234 \(2021\)."). In people with T2D and CKD, dulaglutide compared to insulin glargine correspondingly lowered circulating and urinary fibrotic biomarkers[15](https://www.nature.com/articles/s41591-026-04674-2#ref-CR15 "Tuttle, K. R. et al. Indicators of kidney fibrosis in patients with type 2 diabetes and chronic kidney disease treated with dulaglutide. Am. J. Nephrol. 54, 74–82 \(2023\)."). The aim of the REMODEL trial (REnal MODE of action of semagLutide in people with type 2 diabetes and chronic kidney disease; ClinicalTrials.gov registration: [NCT04865770](https://clinicaltrials.gov/ct2/show/NCT04865770)) was to identify kidney-specific mechanisms of action for semaglutide and establish a new framework for mechanistic trials in CKD. To elucidate the therapeutic mechanisms of semaglutide, REMODEL employed a pathophysiologically integrative design including functional magnetic resonance imaging (MRI), histology and molecular profiling of the kidney in a population analogous to the FLOW trial ([NCT03819153](https://clinicaltrials.gov/ct2/show/NCT03819153))[16](https://www.nature.com/articles/s41591-026-04674-2#ref-CR16 "Cherney, D. Z. I. et al. Rationale, design and baseline characteristics of REMODEL, a mechanism-of-action trial with semaglutide in people with type 2 diabetes and chronic kidney disease. Nephrol. Dial. Transpl. 40, 2182–2192 \(2025\)."),[17](https://www.nature.com/articles/s41591-026-04674-2#ref-CR17 "Pruijm, M. et al. REMODELing mechanistic trials for kidney disease: a multimodal, tissue-centered approach to understand the renal mechanism of action of semaglutide. Kidney Int. 109, 6–16 \(2026\)."). A distinctive feature of REMODEL was the inclusion of paired kidney biopsies for single-nucleus RNA sequencing (snRNAseq) and spatial transcriptomics, enabling high-resolution mapping of the effects of semaglutide on kidney cell populations and cell-to-cell interactions. ## Results ### Participant characteristics Between April 2021 and October 2023, 106 participants were randomized at 28 sites in 8 countries (semaglutide, 71; placebo, 35) and included in the analyses (Fig. [1](https://www.nature.com/articles/s41591-026-04674-2#Fig1)). Baseline characteristics were balanced between randomized groups and similar to FLOW (Table [1](https://www.nature.com/articles/s41591-026-04674-2#Tab1) and Extended Data Table [1](https://www.nature.com/articles/s41591-026-04674-2#Tab2)): mean ± standard deviation (s.d.) age was 65.3 ± 9.9 years; 23.6% were women (_n_ /_N_ = 25/106), eGFR-creatinine was 51.1 ± 10.4 ml min−1 per 1.73 m2, median urinary albumin-to-creatinine ratio (UACR) was 187.3 mg g−1 (interquartile range 60.5–546.4), body weight was 89.6 ± 18.9 kg, body mass was index 30.8 ± 5.7 kg m−2 and glycated hemoglobin was 7.1 ± 0.9%. Renin-angiotensin-system inhibitors were used by 99.1% (_n_ /_N_ = 105/106), and sodium–glucose cotransporter-2 (SGLT2) inhibitors were used by 39.6% (_n_ /_N_ = 42/106). The 33 participants (22 semaglutide, 11 placebo) who underwent kidney biopsy had baseline characteristics similar to those of the full trial population except that SGLT2 inhibitors were used by 54.5% (_n_ /_N_ = 18/33). **Fig. 1: Participant disposition.** ![Fig. 1: Participant disposition.](https://media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41591-026-04674-2/MediaObjects/41591_2026_4674_Fig1_HTML.png) [Full size image](https://www.nature.com/articles/s41591-026-04674-2/figures/1) Investigator withdrawal could be initiated at any point during the trial based on the investigator’s discretion for safety, behavioral, compliance or administrative reasons. Completed 52 weeks of treatment indicates completion of the randomized treatment period through the week-52 end-of-treatment visit. Completed study indicates completion of all study phases, including the subsequent 5-week follow-up period and the end-of-trial visit. **Table 1 Cha
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