FIND-CKD Expands Finerenone Evidence Beyond Diabetic CKD, With Rajiv Agarwal, MD

Finerenone (Kerendia) slowed the rate of estimated glomerular filtration rate (eGFR) decline and reduced kidney and cardiovascular events among adults with chronic kidney disease (CKD) without diabetes, according to late-breaking phase 3 FIND-CKD data presented at the 63rd European Renal Association (ERA) Congress and published in the New England Journal of Medicine.

The findings represent the first randomized placebo-controlled evidence evaluating finerenone in adults with CKD without diabetes, “It really removes the need to extrapolate from diabetic trials,” Rajiv Agarwal, MD, professor emeritus of medicine at Indiana University School of Medicine and staff physician at the Richard L. Roudebush VA Medical Center, told HCPLive.

In FIND-CKD, the mean annual rate of change in eGFR from baseline to month 32 was −3.3 mL/min/1.73 m² with finerenone compared with −4.0 mL/min/1.73 m² with placebo, corresponding to a 0.7 mL/min/1.73 m² slower decline with finerenone (95% Confidence Interval [CI], 0.3-1.1; P < .001).

What Is Finerenone?

Finerenone is a selective nonsteroidal mineralocorticoid receptor antagonist that reduces mineralocorticoid receptor overactivation, a pathway associated with inflammation, fibrosis, and kidney injury.

Previous phase 3 trials demonstrated kidney and cardiovascular benefits with finerenone among adults with CKD associated with type 2 diabetes. FIND-CKD was designed to determine whether those benefits extended to adults with CKD without diabetes.

Why Evaluate CKD Without Diabetes?

Although diabetes is a leading cause of CKD, a substantial proportion of patients with CKD do not have diabetes and historically have had fewer disease-modifying treatment options.

“Diabetic patients are not a niche group,” Agarwal said, noting that approximately 50% to 70% of CKD cases occur in adults without diabetes.

Beyond RAS blockade and SGLT2 inhibitors, these patients have had limited therapies with demonstrated kidney outcome benefits.

“The nonsteroidal MRA mechanism is not diabetes specific,” Agarwal said.

FIND-CKD Trial Design and Results

The phase 3 international, double-blind trial enrolled 1584 adults with CKD receiving maximally tolerated RAS blockade. Participants were randomized to finerenone (n = 793) or placebo (n = 791).

At baseline, mean eGFR was approximately 47 mL/min/1.73 m² in both groups.

After an initial increase in eGFR during the first 3 months, participants receiving finerenone experienced a slower chronic decline in kidney function.

At month 32, mean eGFR was 39.4 mL/min/1.73 m² with finerenone and 38.1 mL/min/1.73 m² with placebo.

Although the difference in annual eGFR slope was 0.7 mL/min/1.73 m², Agarwal emphasized that sustained changes in eGFR slope can be clinically meaningful because eGFR slope is a validated surrogate marker for kidney disease progression.

The composite kidney-cardiovascular outcome occurred in 13.9% of participants receiving finerenone compared with 16.9% receiving placebo (HR, 0.77; 95% CI, 0.60-0.99; P = .04).

Supporting Evidence Across CKD Populations

Agarwal noted that findings from FIND-CKD were further supported by an individual patient-level meta-analysis published in The Lancet, which pooled data from FIND-CKD and previous phase 3 finerenone trials in adults with type 2 diabetes and CKD.

Across more than 14,500 participants, finerenone reduced the composite kidney outcome by 24% and the composite cardiovascular outcome by 20%, strengthening the evidence that mineralocorticoid receptor blockade provides benefits beyond diabetic CKD.

Safety Findings

Safety findings were consistent with previous studies of finerenone.

Hyperkalemia occurred more frequently with finerenone, but few participants discontinued treatment or required hospitalization due to hyperkalemia. Rates of acute kidney injury were between groups.

Clinical Implications

FIND-CKD provides randomized evidence that finerenone may slow CKD progression among adults without diabetes, expanding the potential role of mineralocorticoid receptor antagonism across a broader CKD population.