Key result
Finerenone plus RASi is linked to a ~54% urinary total protein reduction, outperforming either monotherapy.
Why the study?
The role of finerenone in IgA nephropathy patients who have discontinued renin-angiotensin system inhibitor therapy remains poorly defined.
Does finerenone improve proteinuria in patients with primary IgA nephropathy after RASi discontinuation compared to RASi monotherapy?
Cohort (n=258)
Yes
Does finerenone improve proteinuria in patients with primary IgA nephropathy after RASi discontinuation compared to RASi monotherapy?
Finerenone monotherapy provides similar short-term proteinuria reduction to RASi monotherapy in IgA nephropathy, while combination therapy offers superior antiproteinuric efficacy.
Finerenone after RASi discontinuation yields proteinuria reduction comparable to RASi alone in IgAN; leaves open its role pending randomized trials.
Background Finerenone has emerged as a promising therapeutic agent for IgA nephropathy (IgAN). The role of finerenone in IgAN patients who have discontinued renin‐angiotensin system inhibitor (RASi) therapy remains poorly defined. Methods This retrospective, multicentre cohort study enrolled patients with primary IgAN who received finerenone and/or RASi treatment. Participants were categorised into three groups: the finerenone plus RASi, finerenone (after RASi discontinuation) and RASi groups. All participants had a baseline estimated glomerular filtration rate (eGFR) ≥ 25 mL/min/1.73 m 2 and urinary total protein (UTP) ≥ 0.5 g/day. The primary outcomes included the percentage change in UTP from baseline and the rate of significant response (defined as ≥ 50% reduction in UTP and < 20% increase in serum creatinine). Results Following 1:1:1 propensity score matching, a total of 258 patients were analysed, with 86 in each group. At 12 months, UTP decreased by 32.24% in the finerenone group and 34.35% in the RASi group ( p = 0.220). The finerenone plus RASi group achieved a significantly greater reduction of 54.43% compared with either monotherapy group (both p < 0.01). Kaplan–Meier analysis confirmed that the finerenone plus RASi group achieved superior significant response rates compared with either monotherapy group (both log‐rank p = 0.001). No significant difference was observed between the RASi and finerenone groups (log‐rank p = 0.856). Although the finerenone plus RASi group exhibited a numerically steeper total eGFR decline (−1.48 vs. −0.44 vs. −0.52 mL/min/1.73 m 2 /year) and a greater increase in the chronic eGFR slope (0.66 vs. 0.37 vs. 0.49 mL/min/1.73 m 2 /year), neither difference reached statistical significance compared with the finerenone or RASi groups. The incidence of adverse events was comparable across all three groups. Conclusion Finerenone achieved short‐term proteinuria reductions in RASi discontinued IgAN patients similar to those achieved with RASi monotherapy. Finerenone combined with RASi enhanced antiproteinuric efficacy while maintaining safety.
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Zeng et al. (2026) conducted a cohort in IgA nephropathy (n=258). Finerenone plus RASi vs. Finerenone monotherapy and RASi monotherapy was evaluated on Percentage change in urinary total protein (UTP) from baseline and rate of significant response (p=<0.01). Finerenone combined with RASi achieved a 54.43% reduction in urinary total protein at 12 months, significantly greater than finerenone (32.24%) or RASi (34.35%) monotherapy (both P<0.01).
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