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MRAs in diabetic kidney disease

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Effect of MRAs on Chronic Kidney Disease Outcomes in Type 2 Diabetes


Meet our Panelists

Dr. David Cherney
David Cherney, MD CM PhD FRCPC Professor of Medicine, University of Toronto Clinician Scientist, Division of Nephrology, University Health Network Senior Scientist, Toronto General Hospital Research Institute Director, Renal Physiology Laboratory, University Health Network Toronto, ON
Dr. Adeera Levin
Adeera Levin, MD FRCPC FCAHS CM Professor of Medicine, University of British Columbia Head Division of Nephrology Executive Director BC Renal Consulting Nephrologist St Paul’s Hospital Vancouver, BC
Dr. George Bakris
George L. Bakris, MD F.A.S.N. F.A.H.A. Professor of Medicine
Director, Am. Heart Assoc Comprehensive Hypertension Center
Chicago, IL
Dr. Rajiv Agarwal
Rajiv Agarwal, MD MS FASN Professor of Medicine,
Indiana University School of Medicine
Indianapolis, IN

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Journal link | Visual Abstract

Finerenone, a nonsteroidal, selective mineralocorticoid receptor antagonist, reduced albuminuria in short-term trials involving patients with chronic kidney disease (CKD) and type 2 diabetes. However, its long-term effects on kidney and cardiovascular outcomes are unknown.


In this double-blind trial, we randomly assigned 5734 patients with CKD and type 2 diabetes in a 1:1 ratio to receive finerenone or placebo. Eligible patients had a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of 30 to less than 300, an estimated glomerular filtration rate (eGFR) of 25 to less than 60 ml per minute per 1.73 m2 of body-surface area, and diabetic retinopathy, or they had a urinary albumin-to-creatinine ratio of 300 to 5000 and an eGFR of 25 to less than 75 ml per minute per 1.73 m2. All the patients were treated with renin–angiotensin system blockade that had been adjusted before randomization to the maximum dose on the manufacturer’s label that did not cause unacceptable side effects. The primary composite outcome, assessed in a time-to-event analysis, was kidney failure, a sustained decrease of at least 40% in the eGFR from baseline, or death from renal causes. The key secondary composite outcome, also assessed in a time-to-event analysis, was death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure.


During a median follow-up of 2.6 years, a primary outcome event occurred in 504 of 2833 patients (17.8%) in the finerenone group and 600 of 2841 patients (21.1%) in the placebo group (hazard ratio, 0.82; 95% confidence interval [CI], 0.73 to 0.93; P=0.001). A key secondary outcome event occurred in 367 patients (13.0%) and 420 patients (14.8%) in the respective groups (hazard ratio, 0.86; 95% CI, 0.75 to 0.99; P=0.03). Overall, the frequency of adverse events was similar in the two groups. The incidence of hyperkalemia-related discontinuation of the trial regimen was higher with finerenone than with placebo (2.3% and 0.9%, respectively).


In patients with CKD and type 2 diabetes, treatment with finerenone resulted in lower risks of CKD progression and cardiovascular events than placebo. (Funded by Bayer; FIDELIO-DKD number, NCT02540993)