Clinical Benefits of Kerendia (Finerenone)
Kerendia (finerenone) provides dual cardiorenal protection in patients with type 2 diabetes and chronic kidney disease, reducing both kidney disease progression by 23% and cardiovascular events by 14%, making it a critical addition to standard therapy for patients with persistent albuminuria despite maximum-tolerated RAS inhibitor therapy. 1
Kidney Protection Benefits
Finerenone delivers substantial kidney-protective effects across the spectrum of diabetic kidney disease:
Reduces kidney failure requiring dialysis or transplantation by 36% (HR 0.64,95% CI 0.41-0.995), representing a clinically meaningful delay in progression to end-stage kidney disease 2, 3
Decreases the composite kidney outcome by 18% (kidney failure, sustained ≥40% eGFR decline, or renal death; HR 0.82,95% CI 0.73-0.93), as demonstrated in the FIDELIO-DKD trial 1
Reduces the composite kidney outcome by 23% (kidney failure, sustained ≥57% eGFR decrease, or renal death; HR 0.77,95% CI 0.67-0.88) in the pooled FIDELITY analysis of over 13,000 patients 1
Improves proteinuria and glomerular filtration rate when used alone or in combination with SGLT2 inhibitors 4
Cardiovascular Protection Benefits
Finerenone provides comprehensive cardiovascular risk reduction beyond kidney protection:
Reduces composite cardiovascular outcomes by 14% (cardiovascular death, nonfatal MI, nonfatal stroke, or heart failure hospitalization; HR 0.86,95% CI 0.78-0.95) in the pooled FIDELITY analysis 1
Decreases cardiovascular events by 13% (HR 0.87,95% CI 0.76-0.98) in the FIGARO-DKD trial, which specifically enrolled patients with less advanced kidney disease 1
Reduces heart failure hospitalizations by 29% (HR 0.71,95% CI 0.56-0.90), a particularly important benefit given the high burden of heart failure in this population 2, 3
Prevents progression from asymptomatic stage A heart failure to symptomatic incident heart failure, reducing the risk of new-onset heart failure in patients without symptomatic HFrEF 1, 5
Lowers sudden cardiac death by 25% (HR 0.75,95% CI 0.57-0.996; P = 0.046), addressing a critical cause of mortality in diabetic kidney disease 6
Mortality Benefits
Finerenone demonstrates significant mortality reduction in on-treatment analyses:
Reduces all-cause mortality by 18% (HR 0.82,95% CI 0.70-0.96; P = 0.014) in on-treatment analysis of the FIDELITY population 6
Decreases cardiovascular mortality by 18% (HR 0.82,95% CI 0.67-0.99; P = 0.040) in on-treatment analysis, with cardiovascular-related mortality being the most common cause of death in this population 6
Improves quality of life in patients with diabetic renal disease, as demonstrated in clinical research 4
Patient Population and Treatment Positioning
The benefits of finerenone apply to a broad spectrum of patients with diabetic kidney disease:
Indicated for patients with type 2 diabetes, CKD stages 2-4 (eGFR 25-90 mL/min/1.73 m²), and persistent albuminuria (UACR ≥30 mg/g) despite maximum-tolerated RAS inhibitor therapy 1
Positioned as additional risk-based therapy after RAS inhibitors and SGLT2 inhibitors in the treatment algorithm, or as an alternative when SGLT2 inhibitors are not tolerated 1
Can be safely added to SGLT2 inhibitors for complementary cardiorenal protection, though definitive data on combined benefits remain limited 2
Benefits are consistent across all KDIGO risk groups, with effects on mortality similar regardless of baseline kidney disease severity 6
Safety Profile
Finerenone has a favorable safety profile compared to steroidal mineralocorticoid receptor antagonists:
Hyperkalemia occurs more frequently (14% vs 6.9% with placebo), but permanent discontinuation rates remain low at only 1.7% vs 0.6% over 3 years 1, 5
No deaths attributed to hyperkalemia occurred in either the FIDELIO-DKD or FIGARO-DKD trials despite the increased incidence 2, 3
Does not cause gynecomastia, unlike spironolactone, representing a significant tolerability advantage 4
Requires potassium monitoring at baseline (must be ≤4.8 mmol/L to initiate), at 1 month, then every 4 months during maintenance therapy 5
Clinical Implementation
The guideline-based approach to finerenone use follows a clear algorithm:
Start finerenone 10 mg once daily if eGFR 25-60 mL/min/1.73 m², or 20 mg once daily if eGFR >60 mL/min/1.73 m² 1, 5
Uptitrate from 10 mg to 20 mg after 1 month if serum potassium remains ≤4.8 mmol/L and eGFR is stable 1, 5
Hold finerenone if potassium >5.5 mmol/L, restart at 10 mg daily when potassium returns to ≤5.0 mmol/L 5
Continue finerenone until dialysis or transplant in patients who maintain appropriate potassium levels and tolerate therapy 5
Common Pitfalls to Avoid
Do not permanently discontinue finerenone for a single episode of potassium >5.5 mmol/L—temporary interruption with dose reduction upon restart successfully manages most cases 5
Do not initiate finerenone before optimizing RAS inhibitor therapy—patients must be on maximum-tolerated doses of ACE inhibitor or ARB first 1, 5
Do not overlook the cardiovascular benefits—finerenone is not merely an antiproteinuric agent but provides substantial cardiovascular risk reduction including heart failure and sudden cardiac death 1, 6
Do not assume SGLT2 inhibitors and finerenone are interchangeable—they have complementary mechanisms and can be used together for additive cardiorenal protection 1, 2