Finerenone in hypertensive non-diabetic chronic kidney disease: a FIND-CKD subgroup analysis

Hypertension is a common attributable cause of chronic kidney disease (CKD). Mineralocorticoid receptor overactivation can lead to hypertension and contributes to CKD progression. In FIND-CKD, finerenone reduced kidney function decline in participants with CKD without diabetes. This prespecified FIND-CKD analysis assessed finerenone efficacy and safety in participants with hypertensive nephropathy.

Adults with estimated glomerular filtration rate (eGFR) 25-<90 mL/min/1.73 m2 and urinary albumin-to-creatinine ratio (UACR) 200-3500 mg/g were randomized 1:1 to once-daily finerenone or placebo. Hypertensive nephropathy was investigator-reported. Total eGFR slope from baseline to Month 32 was assessed, along with a kidney-cardiovascular composite of sustained ≥57% eGFR decline, kidney failure, hospitalization for heart failure, or cardiovascular death.

Of 1584 randomized participants, 459 (29.0%) had hypertensive nephropathy. Mean blood pressure (± SD) was 134/80 ± 14/10 mmHg, mean eGFR was 44 ± 15 mL/min/1.73 m2, median UACR was 797 mg/g (Q1, Q3: 566, 1247). In participants with hypertensive nephropathy, finerenone slowed total eGFR decline versus placebo by 0.65 mL/min/1.73 m2/year (95% CI: 0.02, 1.29; P = .044) and was associated with a reduction in composite kidney-cardiovascular outcome events (HR: 0.61; 95% CI: 0.38, 0.99; P = .045). These effects were consistent irrespective of baseline systolic blood pressure (SBP) (P-interaction: eGFR slope, 0.96; composite outcome, 0.91). Finerenone reduced SBP by -3.5 mmHg and UACR by 33% at Month 6 vs placebo. Hyperkalaemia occurred more frequently with finerenone (17.1%) than placebo (9.8%); related discontinuation was uncommon (1.3% vs 0.0%, respectively).

Finerenone slowed eGFR decline and reduced kidney-cardiovascular outcome risk in participants with hypertensive nephropathy, supporting its use in this population. ClinicalTrials.gov registration: NCT05047263.