{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T15:53:33Z","timestamp":1790006013739,"version":"4.0.1"},"reference-count":28,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T00:00:00Z","timestamp":1758067200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,10,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Large-scale clinical trials have shown that finerenone reduces the urinary albumin-to-creatinine ratio (UACR) and slows estimated glomerular filtration rate (eGFR) decline, thereby inhibiting a composite cardiovascular and kidney endpoint. However, the efficacy and safety of finerenone in clinical practice remain unknown. This study evaluated eGFR decline and changes in UACR as efficacy endpoints and changes in the serum potassium level as a safety endpoint in patients with diabetic kidney disease (DKD).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>This retrospective observational study was conducted in a real-world clinical setting and included patients with DKD. Eligible patients were those diagnosed with chronic kidney disease stage G1 to G4 who had a UACR of \u226530\u00a0mg\/gCr while taking a renin\u2013angiotensin system inhibitor and who had initiated finerenone. Endpoints included changes in the eGFR slope, UACR, other urinary biomarkers, laboratory and vital parameters, and adverse events.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The analysis included 120 patients. Finerenone significantly improved the rate of eGFR decline from \u20134.99 (\u20135.75, \u20134.23) to \u20130.59 (\u20131.24, 0.07) mL\/min\/1.73\u00a0m2\/year (P\u00a0&amp;lt;\u00a0.0001). UACR also decreased significantly after finerenone treatment from 908 to 487\u00a0mg\/gCr (P\u00a0&amp;lt;\u00a0.0001). Finerenone improved the eGFR slope across all baseline eGFR and albuminuria categories. The rate of eGFR decline improved regardless of whether sodium\u2013glucose cotransporter 2 inhibitor therapy was used concomitantly. Symptomatic hypotension, acute kidney injury and hyperkalemia leading to drug discontinuation were uncommon.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>This real-world analysis suggests that finerenone may improve the eGFR slope in patients with DKD without causing significant hyperkalemia, regardless of baseline eGFR and albuminuria values.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ckj\/sfaf292","type":"journal-article","created":{"date-parts":[[2025,9,20]],"date-time":"2025-09-20T06:16:12Z","timestamp":1758348972000},"source":"Crossref","is-referenced-by-count":8,"title":["Real-world analysis of the impact of finerenone on estimated glomerular filtration rate and albuminuria in patients with diabetic kidney disease"],"prefix":"10.1093","volume":"18","author":[{"given":"Kiyomi","family":"Ichijo","sequence":"first","affiliation":[{"name":"Nihon University School of Medicine Division of Nephrology, Hypertension and Endocrinology, Department of Medicine, , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryo","family":"Yamaguchi","sequence":"additional","affiliation":[{"name":"Nihon University School of Medicine Division of Nephrology, Hypertension and Endocrinology, Department of Medicine, , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyuki","family":"Takashima","sequence":"additional","affiliation":[{"name":"Nihon University School of Medicine Division of Nephrology, Hypertension and Endocrinology, Department of Medicine, , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroki","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Nihon University School of Medicine Division of Nephrology, Hypertension and Endocrinology, Department of Medicine, , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takashi","family":"Maruyama","sequence":"additional","affiliation":[{"name":"Nihon University School of Medicine Division of Nephrology, Hypertension and Endocrinology, Department of Medicine, , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masanori","family":"Abe","sequence":"additional","affiliation":[{"name":"Nihon University School of Medicine Division of Nephrology, Hypertension and Endocrinology, Department of Medicine, , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2025,9,17]]},"reference":[{"key":"2025102105413271200_bib1","doi-asserted-by":"publisher","first-page":"378","DOI":"10.3390\/jcm11020378","article-title":"Therapeutic advances in diabetic nephropathy","volume":"11","author":"Sawaf","year":"2022","journal-title":"J Clin 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