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Finerenone Shows Promise in IgAN: Reduced Proteinuria, Stable Kidney Function

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A retrospective cohort in finerenone showed nearly 40% proteinuria reduction at 8 months and stable eGFR in patients with IgA nephropathy.

New research on finerenone treatment in patients with IgA nephropathy (IgAN) receiving full supportive care has highlighted a significant reduction in the protein-to-creatinine ratio and stable estimated glomerular filtration rate (eGFR) during follow-up.1

“Our previous study established that high levels of urinary sodium excretion, a surrogate for dietary sodium intake, were associated with poor renal outcomes in patients with IgA nephropathy,” wrote study investigator Jianghua Chen, the director emeritus and professor in the Kidney Disease Center, the First Affiliated Hospital of Zhejiang University, School of Medicine, and colleagues. “Finerenone may protect renal tissue by inhibiting the reabsorption of sodium ions by renal tubules, which need further mechanistic studies, such as Finerenone with SGLT2 inhibitor or more detailed mechanistic studies to clarify the protective pathway in IgA nephropathy.1

Finerenone is a nonsteroidal, selective mineralocorticoid receptor antagonist. In July 2021, the US Food and Drug Administration (FDA) approved the therapy to reduce the risk of sustained eGFR decline, end-stage kidney disease, cardiovascular death, nonfatal myocardial infarction, and hospitalization for heart failure in adults with chronic kidney disease associated with type 2 diabetes.2,3

Additional findings from the FINE-ONE trial, evaluating patients with type 1 diabetes and chronic kidney disease, were presented at the American Society of Nephrology (ASN) Kidney Week 2025. Investigators' research suggested a protective effect of finerenone on renal function, reduced risk of cardiovascular events, and a statistically significant 25% relative reduction in the urine albumin-to-creatinine ratio compared with the placebo in 6 months.1

To evaluate finerenone’s impact in IgAN, Chen and colleagues conducted a retrospective, single-center analysis with follow-up visits at 2, 4, 6, and 8 months at the First Affiliated Hospital of Zhejiang University School of Medicine.1

All patients had received full-dose renin-angiotensin system (RAS) blockade with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARB) for > 12 weeks. Each patient received finerenone 10 mg daily for ≥3 months and was monitored every 1–3 months.1

The study included 18 patients with IgAN receiving comprehensive supportive therapy, including RAS blockade, blood pressure control, and steroids and/or other immunosuppressive agents. Baseline proteinuria was 0.38 (0.28–0.75) g/g, and the average eGFR was 63.18 ± 22.01 mL/min/1.73 m².1

At 2 and 6 months, investigators observed 28.48% (P = .003) and 31.33% (P = .003) reductions in proteinuria, respectively, compared with baseline. At 8 months, proteinuria decreased 39.69%, falling from 0.38 (0.28–0.75) g/g to 0.24 (0.16–0.47) g/g (P = .02).1

Investigators further noted eGFR fluctuations at 2 and 4 months, 54.99 ± 27.49 mL/min/1.73 m² (P = .42) and 58.77 ± 15.78 mL/min/1.73 m² (P = .34), which were not statistically significant. Values remained stable through 6 and 8 months of treatment.1

“These results suggest that finerenone is a promising therapeutic approach for reducing proteinuria in patients with IgA nephropathy,” investigators concluded.1

References
  1. Yu G, Wang M, Zhang X, et al. Effect of finerenone on proteinuria reduction in IgA nephropathy. Ren Fail. 2025;47(1):2588501. doi:10.1080/0886022X.2025.2588501
  2. ScienceDirect. Finerenone. In: Reference Module in Biomedical Sciences. Elsevier; 2025. https://www.sciencedirect.com/topics/medicine-and-dentistry/finerenone. Accessed December 8, 2025.
  3. McGill J. Finerenone Marks a Breakthrough for Kidney Protection in Type 1 Diabetes, With Janet McGill, MD, MA. HCPLive. November 11, 2025. Accessed December 8, 2025. https://www.hcplive.com/view/finerenone-breakthrough-kidney-protection-type-1-diabetes-mcgill

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