Arrow pointing up
SHARE
STUDY EVALUATES FINERENONE IN CHRONIC KIDNEY DISEASE WITHOUT DIABETES
FIND-CKD found a modest slowing of eGFR decline, along with more hyperkalemia
Straight Healthcare
August 2026
SHARE
Illustration of human kidneys
Finerenone (Kerendia®) is a nonsteroidal mineralocorticoid receptor antagonist (MRA). Aldosterone stimulates sodium and water reabsorption in exchange for potassium in the renal collecting duct, and finerenone blocks this effect. It also blocks mineralocorticoid receptors in nonepithelial tissues, including the heart and blood vessels, which is thought to reduce inflammation and fibrosis. Unlike the steroidal MRAs spironolactone and eplerenone, finerenone's structure is not based on a steroid molecule, so it has no relevant affinity for androgen, progesterone, estrogen, or glucocorticoid receptors. In diabetic kidney disease, finerenone improved outcomes in two large trials: FIDELIO-DKD, where the primary kidney composite occurred in 17.8% of finerenone-treated patients versus 21.1% with placebo (HR 0.82; 95% CI 0.73–0.93; P=0.001), and FIGARO-DKD, which found a reduction in cardiovascular events driven by heart failure hospitalizations. More than half of chronic kidney disease (CKD) occurs in people without diabetes, and whether finerenone helps this population was unknown.

The FIND-CKD trial randomized 1,584 adults without diabetes who had CKD with albuminuria (average eGFR 46.7 ml/min, median UACR 819) to finerenone (10 or 20 mg daily, titrated by eGFR and potassium) or placebo. Nearly all participants (99.7%) were on an ACE inhibitor or ARB, but only 17% were taking an SGLT2 inhibitor. The primary endpoint, total eGFR slope through month 32, was −3.3 ml/min/year with finerenone and −4.0 ml/min/year with placebo (difference 0.7; 95% CI 0.3 to 1.1; P<0.001). A composite of sustained eGFR decline ≥ 57%, kidney failure, heart failure hospitalization, or cardiovascular death occurred in 13.9% and 16.9%, respectively (HR 0.77; 95% CI 0.60–0.99; P=0.04); the cardiovascular portion of that composite was uncommon (1.3% vs 2.0%; HR 0.60; 95% CI 0.27–1.33) and not significant. Hyperkalemia was reported in 17.0% of finerenone-treated patients versus 13.3% with placebo; potassium exceeded 5.5 mmol/L in 18.8% and 12.2%, and hyperkalemia led to discontinuation in 1.5% and 0.1%, respectively.

In the FIND-CKD trial, the effects of finerenone on kidney function were modest, with a 0.7 ml/min/year difference in slope amounting to roughly 2 ml/min over 36 months. Finerenone also lowered systolic blood pressure about 5 mmHg more than placebo, which may account for part of the effect. Enrollment required a baseline potassium ≤ 4.8 mmol/L, and potassium was monitored closely; patients in practice are unlikely to be monitored as carefully, so prescribers should check levels regularly, particularly in this population where reduced eGFR and RAS inhibitor therapy are near-universal. Finally, it remains unclear whether the much less expensive steroidal MRAs, spironolactone and eplerenone, would produce similar results, as no head-to-head trial has been performed.