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Finerenone's expansion into non-diabetic kidney disease is prompting a broader rethink of how chronic kidney disease is measured, mechanistically understood, and treated across its many causes.
On an episode of Don't Miss a Beat recorded at the 10th Annual Heart in Diabetes Meeting, hosts Stephen Greene, MD, meeting co-chair and heart failure specialist at Duke University School of Medicine, and Muthiah Vaduganathan, MD, MPH, codirector of the Center for Cardiometabolic Implementation and cardiologist at Brigham and Women's Hospital, spoke with Katherine Tuttle, MD, professor of medicine at the University of Washington, about the phase 3 FIND-CKD trial and how it informs on the overall role of finerenone (Kerendia) in management of cardiovascular-kidney-metabolic syndrome.
FIND-CKD showed finerenone slowed total estimated glomerular filtration rate (eGFR) slope by 0.7 mL/min/1.73 m² per year versus placebo, irrespective of diagnosis. Much of the discussion focused less on the number and more on why it counts as clinically meaningful.
Drawing on CKD Prognosis Consortium data from hundreds of thousands of patients, Tuttle explained why eGFR slope reliably predicts kidney failure when a trial runs at least 2 years. CKD progresses rather than striking as a discrete event, so the field has moved toward endpoints measurable without waiting for organ failure or death.
On safety, hyperkalemia occurred more often with finerenone than placebo, about 12% versus 3%, though fewer than 1% of patients discontinued. The framing was practical, with background SGLT2 inhibition expected to lower the risk.
Mechanism anchors much of the conversation between Tuttle, Greene, and Vaduganathan.
Tuttle highlighted how glomerular diseases, like IgA nephropathy, are immunologic disorders needing disease-specific therapy, yet all CKD converges on shared final common pathways of inflammation and fibrosis. Broad agents like finerenone target those pathways, making combination therapy the emerging model, pairing treatment of the inciting disease with control of progression.
The group also discussed the field’s trend toward precision nephrology. Protocol biopsies from the Kidney Precision Medicine Project showed only about half of patients labeled as diabetic CKD had classic diabetic nephropathy. A parallel to oncology followed, where deep phenotyping replaced uniform regimens, suggesting not every patient will need every drug.
Tuttle positioned finerenone alongside renin-angiotensin system inhibitors and SGLT2 inhibitors as an emerging pillar for non-diabetic CKD, with GLP-1 receptor agonists and endothelin antagonists possibly to come. A pooled analysis of FIDELIO-DKD, FIGARO-DKD, and FIND-CKD showed roughly 30% reductions in kidney and cardiovascular outcomes and an 11% drop in all-cause mortality. The closing point held the cardiorenal patient often arrives through either specialty's door, making preservation of organ function and quality of life the shared aim.
Relevant disclosures for Tuttle include Alnylam, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GSK, Novo Nordisk, Roche, and Travere Therapeutics. Relevant disclosures for Vaduganathan include Amgen, AstraZeneca, Bayer AG, Boehringer Ingelheim Pharmaceuticals, Cytokinetics, Lexicon, and others. Relevant disclosures for Greene include Amgen, AstraZeneca, Bayer Healthcare Pharmaceuticals, Boehringer Ingelheim Pharmaceuticals, Cytokinetics, and others.