Finerenone Reduces Albuminuria in Type 1 Diabetes and CKD

A phase 3 trial shows the mineralocorticoid receptor antagonist finerenone safely lowers albuminuria in adults with type 1 diabetes.

For Doctors in a Hurry

The efficacy of finerenone for treating chronic kidney disease in patients with type 1 diabetes remains unknown despite proven benefits in type 2 diabetes.
Researchers conducted a phase 3 trial randomizing 242 adults with type 1 diabetes and albuminuria to receive either daily finerenone or a placebo.
At six months, finerenone yielded a 25% greater reduction in urinary albumin-to-creatinine ratio than placebo (95% confidence interval, 0.65 to 0.87; P<0.001).
The authors concluded that finerenone significantly decreases albuminuria in adults with type 1 diabetes and chronic kidney disease compared to a placebo.
These findings suggest finerenone effectively reduces albuminuria in this patient population, though physicians must monitor for hyperkalemia, which affected 10.1% of treated participants.

Expanding Renoprotection Beyond Type 2 Diabetes

Chronic kidney disease remains a leading cause of morbidity and mortality for patients with diabetes, driving a critical need for therapies that slow renal decline [1]. In recent years, the nonsteroidal mineralocorticoid receptor antagonist finerenone has become a cornerstone of guideline-directed medical therapy for patients with type 2 diabetes, consistently demonstrating robust reductions in albuminuria, kidney failure, and cardiovascular events [2, 3, 4]. However, the pivotal trials establishing these renoprotective benefits exclusively enrolled patients with type 2 diabetes, leaving a substantial evidence gap regarding its efficacy and safety in other populations [5]. Because the underlying pathophysiology of diabetic kidney disease shares similarities across diabetes types, researchers have questioned whether these same pharmacological interventions might mitigate renal damage in broader patient groups [5]. A new phase 3 trial now offers the first direct evidence on how finerenone affects kidney parameters in adults with type 1 diabetes, providing clinicians with critical data to guide treatment in this previously unstudied population.

The FINE-ONE Trial Design

To address the clinical gap in treating type 1 diabetes, researchers conducted the FINE-ONE trial (ClinicalTrials.gov number NCT05901831), a phase 3 study funded by Bayer designed to evaluate the renoprotective potential of finerenone in this specific patient population. A total of 242 participants underwent randomization. The investigators enrolled adults who had type 1 diabetes, chronic kidney disease with an estimated glomerular filtration rate (eGFR) of 25 to less than 90 ml per minute per 1.73 square meters of body-surface area, and albuminuria. For inclusion, albuminuria was defined as a urinary albumin-to-creatinine ratio of 200 to less than 5000 (with albumin measured in milligrams and creatinine measured in grams). To ensure any observed benefits were additive to standard medical therapy, all participants were actively receiving an angiotensin-converting-enzyme inhibitor or an angiotensin-receptor blocker. Participants were randomly assigned to receive either matching placebo or finerenone at a dose of 10 or 20 mg per day, depending on their baseline eGFR. The primary outcome was the relative change in the urinary albumin-to-creatinine ratio over a period of 6 months, providing a direct measure of the drug's ability to reduce renal stress and slow disease progression in adults with type 1 diabetes.

Significant Reductions in Albuminuria

The primary efficacy analysis demonstrated that finerenone resulted in a significantly greater decrease in the urinary albumin-to-creatinine ratio than placebo in adults with type 1 diabetes and chronic kidney disease. When evaluating the absolute values, the researchers noted that the median urinary albumin-to-creatinine ratio decreased from 574.6 at baseline to 373.5 at 6 months among participants assigned to receive finerenone. In the control group, the median urinary albumin-to-creatinine ratio decreased from 506.4 to 475.6 among those assigned to receive placebo. Translating these absolute shifts into relative changes, the data showed that over a period of 6 months, the urinary albumin-to-creatinine ratio decreased by 34% with finerenone (geometric mean ratio to baseline, 0.66; 95% confidence interval [CI], 0.60 to 0.73). During the same timeframe, the urinary albumin-to-creatinine ratio decreased by 12% with placebo (geometric mean ratio to baseline, 0.88; 95% CI, 0.79 to 0.98). When comparing the two treatment arms directly, this corresponded to a 25% greater reduction with finerenone than with placebo (geometric mean ratio for finerenone versus placebo, 0.75; 95% CI, 0.65 to 0.87; P<0.001). For clinicians managing diabetic kidney disease, these metrics indicate a substantial reduction in proteinuria, a well-established surrogate marker for slowing renal decline and delaying the onset of end-stage kidney disease.

Safety Profile and eGFR Dynamics

When evaluating the safety profile of the drug, the researchers noted that the most common adverse event was hyperkalemia. This elevation in serum potassium occurred in 12 participants (10.1%) treated with finerenone and in 4 participants (3.3%) receiving placebo. Despite the higher incidence in the active treatment arm, the clinical impact was generally manageable. The data showed that only 2 participants (1.7%) discontinued finerenone because of hyperkalemia. For practicing physicians, this indicates that while routine potassium monitoring remains essential when prescribing mineralocorticoid receptor antagonists, severe hyperkalemia leading to treatment cessation is infrequent. The study also detailed the expected hemodynamic effects of the drug on kidney function. At 6 months, the change in the eGFR was -5.6 ml per minute per 1.73 square meters with finerenone, whereas the change in the eGFR was -2.7 ml per minute per 1.73 square meters with placebo. This translated to a difference in eGFR change between finerenone and placebo of -2.9 ml per minute per 1.73 square meters (95% CI, -5.1 to -0.7). Importantly, this initial decline reflects a reduction in intraglomerular pressure rather than structural kidney damage. The researchers confirmed this reversible hemodynamic effect by observing that eGFR values approached baseline levels during the washout period. This dynamic mirrors the familiar eGFR dip seen when initiating angiotensin-converting-enzyme inhibitors or sodium-glucose cotransporter-2 inhibitors, reassuring clinicians that the acute drop does not signify worsening renal failure but rather a protective offloading of glomerular pressure.

Study Info

Finerenone in Type 1 Diabetes and Chronic Kidney Disease

Hiddo J.L. Heerspink, Andreas L. Birkenfeld, David Z.I. Cherney, Helen M Colhoun, et al.

Journal New England Journal of Medicine

Published March 04, 2026