---
title: "GLP-1 receptor agonists and kidney protection in chronic kidney disease"
id: "pubmed-42820470"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42820470"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42820470/"
doi: "10.1042/CS20261312"
published_at: "2026-10-14T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# GLP-1 receptor agonists and kidney protection in chronic kidney disease
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42820470
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42820470/)
- **DOI:** [10.1042/CS20261312](https://doi.org/10.1042%2FCS20261312)
- **Published At:** 2026-10-14T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The review examined clinical and preclinical evidence for **GLP-1 RAs** as therapies for **chronic kidney disease** (CKD), focusing on cardiovascular and renal outcomes observed in major cardiovascular outcome trials and dedicated CKD studies. - Investigators reported reductions in major adverse cardiovascular events and signals of nephroprotection in people with type 2 diabetes (T2D) and CKD, including slower decline in **eGFR** and reduced **albuminuria**. - The authors described multiple, potentially complementary mechanisms: anti-inflammatory effects (reduced CRP and IL-6 in clinical studies; TNF-α and NF-κB modulation in experimental work), antioxidative pathways, antifibrotic signaling, and direct cellular protection of podocytes and endothelium. - Renal hemodynamic and tubular mechanisms were emphasized: natriuresis via inhibition of proximal Na+/H+ exchanger 3, altered tubuloglomerular feedback, and reported reductions in circulating angiotensin II; tissue-level RAAS modulation remains largely experimental. - Preclinical studies support mitochondrial protection, modulation of autophagy, and reductions in extracellular matrix deposition; however, human mechanistic evidence is limited for these pathways and no causal mediation of clinical kidney benefits has been established. - The review integrates systemic effects—weight loss, improved glycemia, blood pressure reduction, and gut–kidney axis signalling—as potential indirect contributors to kidney outcomes. - The authors evaluated risks and safety; the source did not provide detailed safety outcome data in the abstract and full safety-profile specifics require consultation of the full text. - Key unresolved questions highlighted include the precise mechanisms mediating clinical benefits, the extent of direct renal versus indirect systemic effects, and the need for more human mechanistic studies to link pathways to outcomes.
## Clinical Analysis & Structured Key Points
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[Jan Boeckhaus](https://pubmed.ncbi.nlm.nih.gov/?term=Boeckhaus+J&cauthor_id=42820470)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-1 "Department of Intensive Care, King's College London, Guy's and St Thomas' Hospital, London, U.K.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-2 "Department of Nephrology and Rheumatology, University Medical Center Göttingen, Goettingen, Germany."), [John A Sayer](https://pubmed.ncbi.nlm.nih.gov/?term=Sayer+JA&cauthor_id=42820470)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-3 "Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K.")[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-4 "NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, U.K.")[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-5 "Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K."), [Holly Mabillard](https://pubmed.ncbi.nlm.nih.gov/?term=Mabillard+H&cauthor_id=42820470)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-3 "Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K.")[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#full-view-affiliation-6 "Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K.") Affiliations Expand ### Affiliations * 1 Department of Intensive Care, King's College London, Guy's and St Thomas' Hospital, London, U.K. * 2 Department of Nephrology and Rheumatology, University Medical Center Göttingen, Goettingen, Germany. * 3 Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K. * 4 NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, U.K. * 5 Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K. * 6 Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K. * PMID: **42820470** * PMCID: [ PMC13642989 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13642989/) * DOI: [ 10.1042/CS20261312 ](https://doi.org/10.1042/cs20261312) Item in Clipboard Review # GLP-1 receptor agonists-a potential therapy for chronic kidney disease? Jan Boeckhaus et al. Clin Sci (Lond). 2026. Show details Display options Display options Format Abstract PubMed PMID Clin Sci (Lond) Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Clin+Sci+%28Lond%29%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Clin+Sci+%28Lond%29%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42820470/) . 2026 Oct 14;140(10):2249-2265. doi: 10.1042/CS20261312. ### Authors [Jan Boeckhaus](https://pubmed.ncbi.nlm.nih.gov/?term=Boeckhaus+J&cauthor_id=42820470)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-1 "Department of Intensive Care, King's College London, Guy's and St Thomas' Hospital, London, U.K.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-2 "Department of Nephrology and Rheumatology, University Medical Center Göttingen, Goettingen, Germany."), [John A Sayer](https://pubmed.ncbi.nlm.nih.gov/?term=Sayer+JA&cauthor_id=42820470)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-3 "Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K.")[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-4 "NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, U.K.")[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-5 "Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K."), [Holly Mabillard](https://pubmed.ncbi.nlm.nih.gov/?term=Mabillard+H&cauthor_id=42820470)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-3 "Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K.")[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42820470/#short-view-affiliation-6 "Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K.") ### Affiliations * 1 Department of Intensive Care, King's College London, Guy's and St Thomas' Hospital, London, U.K. * 2 Department of Nephrology and Rheumatology, University Medical Center Göttingen, Goettingen, Germany. * 3 Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K. * 4 NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, U.K. * 5 Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K. * 6 Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K. * PMID: **42820470** * PMCID: [ PMC13642989 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13642989/) * DOI: [ 10.1042/CS20261312 ](https://doi.org/10.1042/cs20261312) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract Chronic kidney disease (CKD) represents a significant health burden worldwide, characterized by a gradual decline in kidney function and increased risk of cardiovascular events. Current therapeutic strategies like inhibition of the renin-angiotensin-aldosterone system or sodium-glucose cotransporter 2 inhibitors (SGLT2i), while beneficial, often fail to fully halt CKD progression, and a significant residual risk of disease progression persists. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), initially developed for the treatment of type 2 diabetes (T2D), have emerged as promising agents with pleiotropic effects extending beyond glycemic control and weight loss. Evidence from major cardiovascular outcome trials and dedicated CKD studies demonstrates that GLP-1 RAs can confer significant cardiovascular and nephroprotective benefits in patients with T2D and CKD. These benefits include reductions in major adverse cardiovascular events, slowing of kidney disease progression (as measured by estimated glomerular filtration rate (eGFR) decline), and decreased albuminuria. The mechanisms underlying these effects are complex and involve multiple pathways, including anti-inflammatory, anti-fibrotic, and antioxidative actions, as well as improvements in hemodynamic parameters. We provide a comprehensive overview of the current clinical and preclinical evidence supporting the use of GLP-1 RAs in CKD. We discuss the proposed mechanisms of action by which GLP-1 RAs exert their nephroprotective effects and explore the potential for these agents to improve kidney outcomes across a broad spectrum of patients with CKD and critically evaluate the potential risks and safety profile associated with GLP-1 RA use. **Keywords:** cardiovascular physiologyscular; chronic kidney disease; glucagon-like peptide-1; nephrology. © 2026 The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement The authors declare that there are no competing interests associated with the manuscript. ## Figures [ ![Figure 1](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9399/13642989/b9669e0b4ae2/cs-140-cs20261312-g1.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9399/13642989/df19b3a9bfe0/cs-140-cs20261312-g1.webp) ** Figure 1. Systems-level mechanisms underlying the renal… ** ** Figure 1. Systems-level mechanisms underlying the renal protective effects of GLP-1 receptor agonists in CKD ** **Figure 1. Systems-level mechanisms underlying the renal protective effects of GLP-1 receptor agonists in CKD** This schematic summarizes the multi-system and renal-specific mechanisms through which GLP-1 RAs may confer nephroprotection in CKD, while distinguishing clinically demonstrated effects from mechanisms supported predominantly by experimental or preclinical evidence. Progressive CKD is characterized by inflammation, oxidative stress, endothelial dysfunction, and fibrosis, which together contribute to albuminuria, podocyte injury, and progressive loss of kidney function. Clinically demonstrated kidney effects of GLP-1 RAs include reductions in albuminuria and kidney disease progression/composite kidney outcomes. GLP-1 RAs attenuate inflammation (**1**), with clinical studies demonstrating reductions in circulating inflammatory markers, including CRP and IL-6. Experimental studies additionally support down-regulation of pro-inflammatory pathways involving TNF-α and NF-κB, together with modulation of macrophage polarization towards an anti-inflammatory M2 phenotype. GLP-1 RAs may inhibit oxidative stress (**2**) by reducing NAD(P)H oxidase activity via cAMP–PKA signaling, resulting in lower ROS levels in glomerular and tubular compartments. In parallel, activation of the Nrf2 pathway may enhance endogenous antioxidant defenses. These oxidative stress pathways are predominantly supported by experimental and preclinical studies. Renal hemodynamic and tubular effects represent a key nephrology-specific mechanism (**3**). GLP-1 RAs promote natriuresis through inhibition of the Na+/H+ exchanger 3 in the proximal tubule, reducing proximal tubular sodium reabsorption and increasing distal sodium delivery. This may activate tubuloglomerular feedback, thereby reducing intraglomerular pressure. GLP-1 RAs may also modulate the RAAS, with human mechanistic studies demonstrating reductions in circulating angiotensin II and experimental studies supporting down-regulation of tissue-level angiotensin II. Together, these hemodynamic and tubular effects may contribute to reductions in albuminuria and slowing of eGFR decline. Fibrotic responses (**4**) may be suppressed through inhibition of TGF-β signaling, with experimental studies demonstrating reductions in fibronectin and collagen deposition and modulation of extracellular matrix turnover. GLP-1 RAs may additionally exert direct cellular protective effects (**5**). These include preservation of podocyte integrity through inhibition of TNF-α/NF-κB signaling and modulation of AMP-activated protein kinase pathways, and protection of endothelial function, including maintenance of endothelial glycocalyx and vascular integrity, which may support glomerular filtration barrier stability. Experimental studies also suggest suppression of endothelial inflammatory pathways, including endothelin-1 and receptor for advanced glycation end-products (RAGE) signaling. Emerging cellular mechanisms include mitochondrial protection, characterized by preservation of mitochondrial membrane potential and integrity, reduced ROS generation, and attenuation of mitochondrial apoptosis. Regulation of autophagy pathways may additionally contribute to cellular homeostasis and protein quality control. Evidence supporting these mitochondrial, podocyte, endothelial, antifibrotic, and autophagy-related mechanisms is predominantly derived from experimental or preclinical studies, with limited human mechanistic data and no established evidence that these pathways mediate the observed clinical kidney benefits. Beyond the kidney, GLP-1 RAs act across interconnected organ systems. Central nervous system and metabolic effects include regulation of appetite and body weight, increased insulin secretion, suppression of glucagon, delayed gastric emptying, and improved glycemic control. These systemic metabolic effects may indirectly reduce kidney injury. Cardiovascular effects include reductions in blood pressure, HF events and MACE, improvements in vascular endothelial function and lipid profiles, and potential anti-atherosclerotic effects. Bidirectional interactions within the cardiorenal axis may therefore contribute to overall kidney protection. Gut-derived signaling through the gut–kidney axis, including modulation of the intestinal microbiome and incretin signaling, represents an additional proposed pathway linking extra-renal GLP-1 RA effects with kidney outcomes. The figure distinguishes the strength of evidence supporting these pathways. Clinically demonstrated kidney effects are shown separately from proposed biological mechanisms. An asterisk (*) denotes mechanisms predominantly supported by experimental or preclinical studies. A double asterisk (**) denotes pathways for which human mechanistic evidence supports reductions in circulating angiotensin II, while evidence for tissue-level angiotensin II/RAAS modulation remains experimental or precl
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