A phase 3 clinical trial has found that finerenone, a nonsteroidal mineralocorticoid receptor antagonist, produces a significantly greater reduction in a key marker of kidney damage compared to placebo in adults with Type 1 diabetes and chronic kidney disease (CKD). The results were published on March 5, 2026 in the New England Journal of Medicine.
The trial, named FINE-ONE and registered on ClinicalTrials.gov as NCT05901831, was funded by Bayer. It is described in the paper as a phase 3 study of the level of evidence required for regulatory submissions and is notable because, until now, finerenone had only been tested and reported to improve kidney and cardiovascular outcomes in people with Type 2 diabetes and CKD. Its efficacy and safety in Type 1 diabetes were, by the authors' own account, previously unknown.
Enrollment was limited to adults meeting a specific and demanding set of criteria: a confirmed diagnosis of Type 1 diabetes, CKD with an estimated glomerular filtration rate (eGFR) between 25 and less than 90 ml per minute per 1.73 m², and albuminuria measured as a urinary albumin-to-creatinine ratio (UACR) of between 200 and less than 5,000. Crucially, all participants had to already be receiving either an ACE inhibitor or an angiotensin-receptor blocker, meaning the trial was testing finerenone on top of the existing standard of care, not instead of it.
A total of 242 adults were randomised. Those assigned to the treatment arm received finerenone at either 10 mg or 20 mg per day, with the dose determined by their kidney function. Those in the control arm received a matching placebo.
The primary outcome of the trial was the relative change in UACR over six months, a measure of how much protein is leaking into the urine, which is both a sign of kidney stress and a predictor of future kidney decline.
At baseline, the median UACR in the finerenone group was 574.6. By six months, it had fallen to 373.5. In the placebo group, the median UACR started at 506.4 and fell only to 475.6, a far smaller change.
Expressed as percentage reductions: finerenone achieved a 34% decrease in UACR (geometric mean ratio to baseline: 0.66; 95% CI, 0.60 to 0.73), while placebo achieved a 12% decrease (geometric mean ratio to baseline: 0.88; 95% CI, 0.79 to 0.98). The net difference between finerenone versus placebo was a 25% greater reduction (geometric mean ratio: 0.75; 95% CI, 0.65 to 0.87; P<0.001), a result that is statistically significant.
The trial also tracked eGFR, a direct measure of how well the kidneys are filtering blood. At six months, eGFR had changed by 5.6 ml per minute per 1.73 m² in the finerenone group, compared with 2.7 ml per minute per 1.73 m² in the placebo group. The between-group difference was 2.9 ml per minute per 1.73 m² (95% CI, 5.1 to -0.7), meaning kidney filtration declined somewhat more in the treatment arm than in the placebo arm over the six months of active treatment.
However, the authors note that eGFR values approached baseline levels during the washout period following the end of treatment.
The most commonly reported adverse event was hyperkalemia elevated K-levels in the blood. This occurred in 12 participants (10.1%) in the finerenone group, compared with 4 participants (3.3%) in the placebo group. Two participants in the finerenone group (1.7%) discontinued the drug specifically because of hyperkalemia.
The paper's conclusion, as stated in the abstract, is direct: in adults with Type 1 diabetes and CKD, finerenone resulted in a significantly greater decrease in UACR than placebo.
The trial was conducted across multiple sites and was a double-blind, randomised, placebo-controlled study. Lead author Hiddo J.L. Heerspink is based at the George Institute for Global Health, University of New South Wales, Sydney, and at the University of Groningen, the Netherlands. The paper lists 20 additional co-authors from institutions across Europe, North America, and Asia, as well as investigators from Bayer. The trial was funded by Bayer, as stated in the published paper.
