Kidney Week

Abstract: TH-PO0480

Finerenone as a Nephroprotective Agent in IgAN: A Prospective Six-Month Pilot Study

Session Information

• Glomerular Diseases: Clinical, Outcomes, and Therapeutics Research - IgAN
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

• Shutov, Evgeny, Botkin Hospital, Moscow, Russian Federation

Evgeny Shutov, MD, DrMed, PhD

• Zykova, Anastasiia, Botkin Hospital, Moscow, Russian Federation

Anastasiia Zykova, MD, PhD

• Pushkar, Ilya, Botkin Hospital, Moscow, Russian Federation

Ilya Pushkar, MD

• Bolshakov, Stepan, Botkin Hospital, Moscow, Russian Federation

Stepan Bolshakov, MD

• Abduvaitova, Nargiza, Botkin Hospital, Moscow, Russian Federation

Nargiza Abduvaitova, MD

• Budaeva, Zalina, Botkin Hospital, Moscow, Russian Federation

Zalina Budaeva, MD

• Natalia, Chernyshova, Botkin Hospital, Moscow, Russian Federation

Chernyshova Natalia

• Dudko, Marina, Botkin Hospital, Moscow, Russian Federation

Marina Dudko, MD, PhD

• Zakharova, Elena, Botkin Hospital, Moscow, Russian Federation

Elena Zakharova, MD, PhD

Background

IgA nephropathy (IgAN) is the most prevalent glomerulonephritis and frequently progresses to end-stage kidney disease (ESKD). Current standard-of-care nephroprotection relies on renin-angiotensin system inhibitors (RASi) and SGLT2 inhibitors (SGLT2i). While the non-steroidal mineralocorticoid receptor antagonist (MRA) finerenone has shown efficacy in diabetic kidney disease, prospective data in non-diabetic IgAN cohorts remain limited.

Methods

This prospective, interventional pilot trial (NCT07056595) enrolled adults with biopsy-proven IgAN. Inclusion criteria included 24-hour urinary albumin excretion (24h-AUE) > 300 mg, eGFR > 20 mL/min, and stable doses of RASi and/or SGLT2i for at least 3 months. Patients requiring immunosuppression were excluded. Participants received finerenone 10 mg/day for 6 months; concomitant therapy adjustments were prohibited. Outcomes included changes in 24h-AUE, serum creatinine, and eGFR.

Results

Thirty-three patients were included (16 female, 17 male, median age 38.5 years [IQR 30.5–47.5]). In the overall cohort, median 24h-AUE significantly decreased from 1128.0 mg (IQR 788.7–1473.5) at baseline to 678.4 mg (IQR 424.5–1395.4) at 6 months (p=0.002). However, nine patients (27.3%) did not respond to treatment. Serum creatinine and eGFR changes were non-significant (median 144.15 versus 140.65 mmol/l, p=0.324; median 54.5 versus 52.5 ml/min, p=0.539) at the end of the follow-up. Two patients—a 30-year-old female (eGFR 30 mL/min at baseline) and a 44-year-old male (eGFR 23 mL/min at baseline)—progressed to ESKD; both had demonstrated severe glomerulosclerosis and interstitial fibrosis on kidney biopsy. Regarding safety, one patient (23-year-old female) developed transient hyperkalemia (potassium 5.6 mmol/L), which resolved two weeks after finerenone discontinuation. No severe hypotension was reported.

Conclusion

Finerenone appears to be an effective nephroprotective agent in IgAN with a favorable safety profile. These results suggest a significant reduction in albuminuria when added to standard-of-care therapy. However, the progression observed in patients with advanced sclerotic lesions suggests that early treatment is critical to optimize clinical outcomes and prevent progression to ESKD.