Finerenone (Kerendia) earned its first regulatory home in diabetic kidney disease, and it is also approved for heart failure with mildly reduced or preserved ejection fraction. It is not approved for chronic kidney disease (CKD) in people without diabetes. Two papers published this week push at that boundary — one trial showing the drug slows kidney decline in patients who do not have diabetes, and a pooled analysis arguing the benefit holds across the CKD spectrum. The non-diabetic indication remains investigational and would require a regulatory decision before it could become an available option.
FIND-CKD (NCT05047263), a Bayer-funded phase 3 trial, randomized 1,584 adults with non-diabetic CKD, albuminuria, and a renin-angiotensin system inhibitor on board: 793 to finerenone and 791 to placebo, per the New England Journal of Medicine report. The trial enrolled a population deliberately selected for lower hyperkalemia risk: per the registry, participants had to have a baseline serum potassium of 4.8 mmol/L or lower, be on a stable, maximally tolerated labelled dose of an ACE inhibitor or ARB for at least four weeks, and not have diabetes (type 1 or 2 diabetes, or an HbA1c of 6.5% or higher, was an exclusion). Those entry criteria matter for reading the results — they cannot simply be generalized to unselected patients.
The primary endpoint — the total eGFR slope, the mean annual change in estimated glomerular filtration rate from baseline to month 32 — favored the drug. eGFR fell by 3.3 mL/min/1.73m² per year on finerenone versus 4.0 on placebo, a difference of 0.7 (95% CI, 0.3 to 1.1; P<0.001).
A prespecified composite of kidney-or-cardiovascular events was also lower with finerenone (hazard ratio 0.77; 95% CI, 0.60 to 0.99; P=0.043). The signal narrows on the components: HR 0.78 (0.60 to 1.01) for the two kidney events and 0.60 (0.27 to 1.33) for the two cardiovascular events — both confidence intervals crossing 1. Hyperkalemia was the most common adverse event: 17.0% of finerenone-treated participants versus 13.3% of placebo-treated participants had it, and it led to hospitalization in 0.9% and 0.6%, respectively — a rate to read against those potassium and background-therapy entry rules, not as a population-wide estimate. Finerenone is contraindicated or hazardous in the setting of hyperkalemia and with certain concomitant drugs (such as strong CYP3A4 inhibitors), and serum potassium and kidney function require monitoring; this is not a treatment decision readers should self-direct.
What the pool adds
The INFINITY analysis, published in The Lancet, combines individual participant data from FIDELIO-DKD, FIGARO-DKD, and FIND-CKD — 14,574 participants across diabetic and non-diabetic CKD. Finerenone cut the composite kidney outcome (kidney failure or a sustained eGFR drop of 57% or more) by 24% versus placebo (HR 0.76; 95% CI, 0.68 to 0.86) and kidney failure alone (HR 0.85; 0.74 to 0.99). The cardiovascular composite fell to HR 0.80 (0.70 to 0.91), with all-cause death at 0.88 (0.79 to 0.99).
Treatment effects on the kidney outcome were consistent regardless of glycaemic status, CKD aetiology, baseline eGFR, albuminuria, or SGLT2-inhibitor use, the authors report.
The trials enrolled selected, albuminuric populations on background therapy with screening potassium ceilings; hyperkalemia remains the trade-off. The authors frame finerenone as a “foundational therapy” across CKD — but for non-diabetic CKD specifically, that is an investigational claim, not a current label. Finerenone is not yet approved for CKD without diabetes; any expansion of its use would await regulatory review, and it is regulators, not the journal article, who will adjudicate both the approval status and the “foundational therapy” framing.