Finerenone slowed kidney decline in CKD without diabetes
In the FIND-CKD trial, non-diabetic patients on finerenone lost kidney function at 3.3 versus 4.0 ml/min/1.73 m² a year — a small edge that extends a diabetes drug to a new group.
| Group | Value (ml/min/1.73 m²) |
|---|---|
| Finerenone | 3.3 (3.1 to 3.6) |
| Placebo | 4 (3.8 to 4.3) |
Finerenone, a kidney-protective drug proven in people with type 2 diabetes, also slowed the loss of kidney function in patients who have chronic kidney disease (CKD) but not diabetes, according to the FIND-CKD trial in the New England Journal of Medicine [s1]. Over 32 months, kidney function fell by 3.3 ml per minute per 1.73 m² a year on finerenone versus 4.0 on placebo — a real but modest difference of 0.7 [s1].
The result fills a specific gap. Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, earned its place in kidney care through trials in diabetic CKD, most prominently FIDELIO-DKD, which showed it improved kidney and cardiovascular outcomes in people with type 2 diabetes [s2]. Whether the same benefit reached patients whose CKD comes from other causes — hypertension, glomerular disease, or unknown origins — had not been tested in a dedicated trial until now [s1].
What the trial did
FIND-CKD, funded by Bayer, randomly assigned adults without diabetes who had CKD and protein in the urine to finerenone or placebo [s1]. Eligibility required an estimated glomerular filtration rate (eGFR) between 25 and less than 90 ml per minute per 1.73 m², a urinary albumin-to-creatinine ratio between 200 and 3500 mg per gram, and background treatment with a renin-angiotensin system inhibitor — the existing standard of care that finerenone was being added on top of [s1]. Participants took finerenone at 10 or 20 mg daily, or a matching placebo [s1].
A total of 1584 participants were randomised, 793 to finerenone and 791 to placebo, and the two groups started from nearly identical kidney function: a mean baseline eGFR of 46.8 ml per minute per 1.73 m² with finerenone and 46.6 with placebo [s1]. The primary outcome was the total eGFR slope — the mean annual rate at which kidney function changed from baseline to month 32 — rather than a count of clinical events, a choice that lets a trial detect a treatment's effect on the disease's trajectory within a few years [s1].
What it found
The mean annual fall in eGFR was 3.3 ml per minute per 1.73 m² with finerenone (95% confidence interval −3.6 to −3.1) and 4.0 with placebo (95% CI −4.3 to −3.8), a difference in slope of 0.7 ml per minute per 1.73 m² (95% CI 0.3 to 1.1; P<0.001) [s1]. A prespecified composite of kidney or cardiovascular events — a 57% or greater drop in eGFR, kidney failure, hospitalisation for heart failure, or cardiovascular death — was less common with finerenone, with a hazard ratio of 0.77 (95% CI 0.60 to 0.99; P=0.04) [s1]. The kidney-only composite gave a hazard ratio of 0.78 (95% CI 0.60 to 1.01) and the cardiovascular-only composite 0.60 (95% CI 0.27 to 1.33), the latter resting on few events and a wide, non-significant interval [s1].
The main safety cost was the one finerenone's mechanism predicts. Hyperkalaemia — a rise in blood potassium — occurred in 135 participants (17.0%) on finerenone versus 105 (13.3%) on placebo, led to stopping the drug in 12 participants (1.5%) versus 1 (0.1%), and led to hospitalisation in 7 (0.9%) versus 5 (0.6%) [s1].
How to read it
The slope difference is statistically clear but clinically modest: 0.7 ml per minute per 1.73 m² per year is a slowing of decline, not a halt, and its value depends on how many years a patient has that decline to slow. The event composite reached significance only narrowly, with an upper confidence bound of 0.99, so the outcome benefit is real but not resounding, and the cardiovascular component is too sparse to stand on its own [s1].
Set against that is a predictable, manageable harm. The excess hyperkalaemia is consistent with how the drug works, and while it rarely forced hospitalisation, it did push more patients off treatment than placebo did — a reminder that finerenone in this population needs the potassium monitoring its diabetic use already demands [s1].
Why it matters
Non-diabetic CKD has had fewer dedicated drug trials than its diabetic counterpart, even though the two share the same trajectory toward dialysis. FIND-CKD widens the evidence for a second protective mechanism beyond the SGLT2 inhibitors that have become standard, discussed on this site in how SGLT2 drugs protect the kidney and heart beyond diabetes and in an individual-patient meta-analysis of empagliflozin's kidney outcomes. Finerenone itself has been moving outward from its diabetic-CKD origins, including into heart failure, as covered in the FINEARTS trial in heart failure with preserved ejection fraction [s1][s2].
What to watch
The near-term questions are about labels and layering: whether regulators broaden finerenone's indication to non-diabetic CKD, and how it is combined with SGLT2 inhibitors and RAS blockers, since each raises potassium and the trio has not been tested together at scale [s1]. Longer follow-up would show whether a slope advantage sustained past 32 months translates into the harder outcomes — dialysis and death — that a two-slope model can only forecast [s1].
This article describes research and is not medical advice. Decisions about kidney-disease treatment are for patients and their treating clinicians.
Sources
- Finerenone in Persons with Chronic Kidney Disease without Diabetes — New England Journal of Medicine, 4 June 2026
- Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes (FIDELIO-DKD) — New England Journal of Medicine, 23 October 2020
Sources
- Finerenone in Persons with Chronic Kidney Disease without Diabetes — New England Journal of Medicine , June 4, 2026
- Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes (FIDELIO-DKD) — New England Journal of Medicine , October 23, 2020
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