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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.<\/jats:p>","DOI":"10.1042\/cs20261312","type":"journal-article","created":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T10:50:19Z","timestamp":1790851819000},"page":"2249-2265","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["GLP-1 receptor agonists\u2014a potential therapy for chronic kidney disease?"],"prefix":"10.1042","volume":"140","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-2021-9255","authenticated-orcid":false,"given":"Jan","family":"Boeckhaus","sequence":"first","affiliation":[{"name":"1Department of Intensive Care, King's College London, Guy's and St Thomas' Hospital, London, U.K."},{"name":"2Department of Nephrology and Rheumatology, University Medical Center G\u00f6ttingen, Goettingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John\u00a0A.","family":"Sayer","sequence":"additional","affiliation":[{"name":"3Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K."},{"name":"4NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, U.K."},{"name":"5Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holly","family":"Mabillard","sequence":"additional","affiliation":[{"name":"3Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, U.K."},{"name":"6Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle upon Tyne, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2026,10,1]]},"reference":[{"key":"2026100106501224000_B1","doi-asserted-by":"publisher","first-page":"1238","DOI":"10.1016\/S0140-6736(16)32064-5","article-title":"Chronic kidney disease","volume":"389","author":"Webster","year":"2017","journal-title":"Lancet"},{"key":"2026100106501224000_B2","doi-asserted-by":"publisher","first-page":"90","DOI":"10.1016\/S0140-6736(25)01942-7","article-title":"Chronic kidney disease","volume":"407","author":"Herrington","year":"2026","journal-title":"Lancet"},{"key":"2026100106501224000_B3","doi-asserted-by":"publisher","first-page":"1228","DOI":"10.1093\/ndt\/gfae027","article-title":"Glomerular hyperfiltration as a therapeutic target for CKD","volume":"39","author":"Kanbay","year":"2024","journal-title":"Nephrol. 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