{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T07:15:51Z","timestamp":1791875751689,"version":"4.3.4"},"reference-count":49,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2023,10,10]],"date-time":"2023-10-10T00:00:00Z","timestamp":1696896000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100004326","name":"Bayer","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004326","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>Investigating the effect of finerenone on liver function, cardiovascular and kidney composite outcomes in patients with chronic kidney disease and type 2 diabetes, stratified by their risk of liver steatosis, inflammation and fibrosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>Post hoc analysis stratified patients (N\u2009=\u200913\u2009026) by liver fibrosis and enzymes: high risk of steatosis (hepatic steatosis index &gt;36); elevated transaminases [alanine transaminase (ALT) &gt;33 (males) and &gt;25\u2009IU\/L (females)]; and fibrosis\u20104 (FIB\u20104) index scores &gt;3.25, &gt;2.67 and &gt;1.30. Liver enzymes were assessed by changes in ALT, aspartate aminotransferase and gamma\u2010glutamyl transferase. Composite kidney outcome was defined as onset of kidney failure, sustained estimated glomerular filtration rate decline \u226557% from baseline over \u22654\u2009weeks or kidney death. Composite cardiovascular outcome was defined as cardiovascular death, non\u2010fatal myocardial infarction, non\u2010fatal stroke or hospitalization for heart failure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      ALT, aspartate aminotransferase and gamma\u2010glutamyl transferase levels were consistent between treatment groups and remained stable throughout. Finerenone consistently reduced the risk of composite kidney outcome, irrespective of altered liver tests. Higher FIB\u20104 score was associated with higher incidence rates of composite cardiovascular outcome. Finerenone reduced the risk of composite cardiovascular outcome versus placebo in FIB\u20104 subgroups by 52% (&gt;3.25), 39% (&gt;2.67) and 24% (&gt;1.30) (\n                      <jats:italic>p<\/jats:italic>\n                      values for interaction\u2009=\u2009.01, .13 and .03, respectively).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Finerenone has neutral effects on liver parameters in patients with chronic kidney disease and type 2 diabetes. Finerenone showed robust and consistent kidney benefits in patients with altered liver tests, and profound cardiovascular benefits even in patients with higher FIB\u20104 scores who were at high risk of developing cardiovascular complications.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.15305","type":"journal-article","created":{"date-parts":[[2023,10,11]],"date-time":"2023-10-11T23:27:29Z","timestamp":1697066849000},"page":"191-200","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Efficacy of finerenone in patients with type 2 diabetes, chronic kidney disease and altered markers of liver steatosis and fibrosis: A\n                    <scp>FIDELITY<\/scp>\n                    subgroup analysis"],"prefix":"10.1111","volume":"26","author":[{"given":"Nikolaos","family":"Perakakis","sequence":"first","affiliation":[{"name":"University Study Center for Metabolic Diseases, Department of Internal Medicine III Carl Gustav Carus University Clinic, TU Dresden  Dresden Germany"},{"name":"University Hospital and Faculty of Medicine, TU Dresden, Dresden, Paul Langerhans Institute Dresden (PLID), Helmholtz Center Munich  Dresden Germany"},{"name":"Neuherberg, German Center for Diabetes Research (DZD e.V.)  Neuherberg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan R.","family":"Bornstein","sequence":"additional","affiliation":[{"name":"University Study Center for Metabolic Diseases, Department of Internal Medicine III Carl Gustav Carus University Clinic, TU Dresden  Dresden Germany"},{"name":"University Hospital and Faculty of Medicine, TU Dresden, Dresden, Paul Langerhans Institute Dresden (PLID), Helmholtz Center Munich  Dresden Germany"},{"name":"Neuherberg, German Center for Diabetes Research (DZD e.V.)  Neuherberg Germany"},{"name":"Diabetes and Nutritional Sciences, King's College London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1407-9023","authenticated-orcid":false,"given":"Andreas L.","family":"Birkenfeld","sequence":"additional","affiliation":[{"name":"Neuherberg, German Center for Diabetes Research (DZD e.V.)  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