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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Nephrol. Sep 25, 2026; 15(3): 121881
Published online Sep 25, 2026. doi: 10.5527/wjn.121881
Letter to the Editor: Finerenone and proteinuria in diabetic kidney disease
Sotiris Gavriil, Vaia D Raikou
Vaia D Raikou, Department of Nephrology, Doctors’ General Clinic, Athens 11257, Greece
Sotiris Gavriil, Department of Weight-Surgery, Doctors’ Hospital, Athens 11257, Greece
Author contributions: Raikou VD and Gavriil S contributed to research plan; Raikou VD contributed to manuscript writing; Gavriil S contributed to approval of written manuscript.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Vaia D Raikou, PhD, Chief, Department of Nephrology, Doctors’ General Clinic, 26 Kefallinias, Athens 11257, Greece. vraikou@med.uoa.gr
Received: April 7, 2026
Revised: April 27, 2026
Accepted: May 13, 2026
Published online: September 25, 2026
Processing time: 132 Days and 11.2 Hours
Abstract

Most patients with diabetic kidney disease (DKD) suffer from proteinuria. Finerenone, a novel nonsteroidal mineralocorticoid receptor antagonist acts as anti-inflammatory factor reducing the kidney inflammation and fibrotic pathways, which are overactive in patients with advanced proteinuria. The study by Pasari et al, published in the recent issue of the World Journal of Nephrology, correlated the greater reduction of albuminuria with the higher baseline albuminuria using finerenone. However, heterogeneity, disproportion and variability in response using finerenone for the reduction of proteinuria has been observed. Patients with persistent proteinuria despite the optimal renin-angiotensin-aldosterone system blockage, sodium-glucose co-transporter -2 inhibitors and finerenone, remain at high risk for renal and cardiovascular events. More factors including the novel functions of histone lactylation possibly are involved in the deterioration of albuminuria in DKD. It may need combined and intensive therapy with an additional healthy lifestyle. More pharmacogenomic trials, proteomic analyses in long-term real-world cohorts need to clarify the pathogenetic mechanisms related to proteinuria in DKD.

Keywords: Diabetic nephropathy; Proteinuria; Kidney inflammation; Finerenone; Cardiovascular events

Core Tip: Diabetic nephropathy is mainly characterized by proteinuria, which contributes to renal progression and cardiovascular complications. Finerenone, a novel nonsteroidal mineralocorticoid receptor antagonist, can reduce proteinuria with a dependance on initial baseline proteinuria, despite its effect may be disproportional and variant. More factors including genetics or epigenetics may be involved in diabetic kidney pathology, because of which proteinuria persists.

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