03719nam a2200337 4500001000800000007000300008008004100011040000800052041000800060100004100068245007100109300002300180520258400203650003302787650003802820650003802858650003202896700003002928700002702958700003202985700003003017700003303047700003003080700003203110700002403142700003003166700002703196773011003223942003103333999001703364ESSALUDta t pe ||||| |||| 00| 0 spa d aBMG aeng aHeerspink, Hiddo J. L.eAutor954043 aFinerenone in persons with chronic kidney disease without diabetes apáginas: 533-545 aBackground: In randomized trials, finerenone, a nonsteroidal mineralocorticoid receptor antagonist, improved kidney and cardiovascular outcomes in patients with type 2 diabetes and chronic kidney disease (CKD). Whether finerenone has similar effects in patients without diabetes who have CKD is unknown. Methods: We randomly assigned adults without diabetes who had CKD (estimated glomerular filtration rate [eGFR], 25 to <90 ml per minute per 1.73 m2 of body-surface area) and albuminuria (urinary albumin-to-creatinine ratio, 200 to ≤3500, with albumin in milligrams and creatinine in grams) and were using a renin–angiotensin system inhibitor to receive finerenone (10 or 20 mg daily) or placebo. The primary outcome was the total eGFR slope (mean annual rate of change in the eGFR from baseline to month 32), assessed with a two-slope linear spline mixed-effects model. Secondary outcomes included a composite of kidney or cardiovascular events (reduction from baseline of at least 57% in the eGFR, kidney failure, hospitalization for heart failure, or death from cardiovascular causes), a composite of the two kidney events, and a composite of the two cardiovascular events. Results: A total of 1584 participants underwent randomization — 793 were assigned to the finerenone group, and 791 to the placebo group. The mean (±SD) baseline eGFR was 46.8±16.2 ml per minute per 1.73 m2 with finerenone and 46.6±16.0 ml per minute per 1.73 m2 with placebo. The mean annual rate of change in the eGFR from baseline to month 32 was −3.3 ml per minute per 1.73 m2 (95% confidence interval [CI], −3.6 to −3.1) with finerenone and −4.0 ml per minute per 1.73 m2 (95% CI, −4.3 to −3.8) with placebo (difference, 0.7; 95% CI, 0.3 to 1.1; P<0.001). Prespecified hierarchical testing showed that the risk of a composite kidney or cardiovascular outcome event was lower with finerenone than with placebo (hazard ratio, 0.77; 95% CI, 0.60 to 0.99; P=0.04); the hazard ratio was 0.78 (95% CI, 0.60 to 1.01) for the composite of the two kidney events and 0.60 (95% CI, 0.27 to 1.33) for the composite of the two cardiovascular events. The most common adverse event was hyperkalemia (135 participants [17.0%] with finerenone and 105 [13.3%] with placebo); hyperkalemia events led to discontinuation of the trial regimen in 12 participants (1.5%) and 1 participant (0.1%), respectively, and to hospitalization in 7 (0.9%) and 5 (0.6%). Conclusions: Among adults with CKD who did not have diabetes, finerenone led to a slower decrease in the eGFR than placebo over 32 months. aCARDIOLOGÍA GENERAL953638 aENFERMEDAD RENAL CRÓNICA932213 aMEDICINA CLÍNICA GENERAL953666 aNEFROLOGÍA GENERAL953655 aNeuen, Brendon L. 954044 aAgarwal, Rajiv 954045 aCherney, David Z.I. 954046 aLam, Carolyn S.P. 954047 aTuttle, Katherine R. 954048 aWanner, Christoph 945757 aSarafidis, Pantelis 954049 aJongs, Niels954050 aSmeijer, J. David 954051 aBrinker, Meike 9540520 022717922644dMassachusetts NEJM GroupoNEJM009tThe New England Journal of Medicine wESSALUDx0028-4793 cARTICULOSe2026-08-14zSQB c22812d22812