Finerenone in IgAN: A Proteinuria Signal Worth Following

Persistent proteinuria is a central challenge in IgA nephropathy (IgAN), even as treatment options expand. A 12-month retrospective study published in Renal Failure adds preliminary evidence that finerenone may have a role in addressing this residual burden. Among adults with biopsy-proven IgAN, treatment was associated with lower urinary protein excretion and stable estimated glomerular filtration rate (eGFR). The findings offer a reason for further investigation, although they do not establish that finerenone prevents kidney disease progression in this population.

Pei and colleagues evaluated 52 adults without diabetes who initiated finerenone at the First Affiliated Hospital of Xiamen University in China. Eligibility required at least 90 days of finerenone treatment; their mean age was 40.6 years, and 71.2% were women. Baseline mean eGFR was approximately 76 mL/min/1.73 m², and median urinary protein excretion was 750 mg/24 hours. Most patients received finerenone 10 mg daily, alongside renin-angiotensin system inhibitors in 86.5% and sodium-glucose cotransporter-2 inhibitors in 50%.

The proteinuria signal emerged gradually. Significant reductions relative to baseline appeared at month 6, and median urinary protein excretion reached 496 mg/24 hours at month 12 (P = 0.003). The median percentage reduction from baseline at month 12 was 29.7%. However, the overall time effect across all visits was not statistically significant in the generalized estimating equation analysis (P = 0.105). This distinction tempers interpretation of the significant comparisons at individual visits.

Remission was also far from universal. Among 32 patients with baseline proteinuria of at least 300 mg/24 hours and available month-12 data, five achieved complete remission and five achieved partial remission, producing an overall response rate of 31.3%. Complete remission required proteinuria below 300 mg/24 hours; partial remission required at least a 50% reduction without reaching complete remission. Both definitions also required an eGFR decrease of no more than 30%.

An exploratory analysis provided another useful signal: proteinuria also declined among patients who were not receiving immunosuppressive therapy. Among the 35 patients in this subgroup with month-12 data, median urinary protein excretion reached 476 mg/24 hours (P = 0.017 versus baseline). This suggests that concurrent immunosuppression was not necessary for the observed association, but it does not isolate finerenone’s contribution from other therapies or disease fluctuations.

Mean eGFR remained essentially unchanged, from 75.99 to 75.04 mL/min/1.73 m² over 12 months (P = 0.873). That stability is encouraging, but without a comparator and longer follow-up, it cannot establish a kidney-protective effect. Safety findings were similarly reassuring within the limits of this cohort: two patients (3.8%) developed hyperkalemia (≥ 5.5 mmol/L), managed with dietary counseling or short-term potassium-binding treatment. No treatment discontinuations or serious adverse events were reported.

For clinicians, the study highlights a potential adjunctive approach that still requires stronger evidence. Finerenone use for IgAN was off-label in this study, and any consideration requires individualized assessment and attention to potassium and kidney function. Only 39 participants had month-12 data, concomitant therapies could explain part of the improvement, and retrospective safety collection may have missed events. Controlled prospective studies will need to determine whether the proteinuria signal translates into durable preservation of kidney function and which patients can benefit.

Reference:
Pei J, Sun X, Xu X, et al. Efficacy and safety of finerenone in adults with IgA nephropathy: a 12-month real-world study. Ren Fail. 2026;48(1):2681246. doi:10.1080/0886022X.2026.2681246