Two-Year Renal Outcomes of Finerenone in Patients with Type 2 Diabetes and Chronic Kidney Disease: A Real-World Observational Study

 

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Two-Year Renal Outcomes of Finerenone in Patients with Type 2 Diabetes and Chronic Kidney Disease: A Real-World Observational Study

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Ryosuke
Nishiura
Ryosuke Nishiura windebll1162@gmail.com Nishiura Hospital Internal medicine Miyakonojo city Japan *
Nozomi Watanabe nozomi_watanabe@med.miyazaki-u.ac.jp University of MIyazaki Cadioavascular physiology, Faculity of Medicine Miyazaki Japan -
 
 
 
 
 
 
 
 
 
 
 
 
 

Finerenone, a novel non-steroidal and selective mineralocorticoid receptor antagonist (MRA), has been shown to reduce albuminuria and is expected to prevent the progression of renal and CV injury by suppressing inflammation and fibrosis associated with excessive mineralocorticoid receptor activation. However, clinical evidence regarding the long-term effects of finerenone on renal outcomes in real-world practice remains limited. This study aimed to evaluate longitudinal changes in renal function over two years following finerenone administration in patients with T2D and CKD.

This retrospective observational study included consecutive 74 patients (M/F: 40/34, aged ≥20 years) with T2D and CKD (estimated glomerular filtration rate [eGFR] >20 mL/min/1.73 m²) who exhibited proteinuria. Laboratory data, including serum creatinine, urinary liver-type fatty acid–binding protein (L-FABP), β2-microglobulin (β2MG), urinary protein-to-creatinine ratio (UPCR), and urinary albumin-to-creatinine ratio (UACR), were collected at 12 months before finerenone initiation, baseline, and at 3, 6, 12, and 24 months after initiation. The eGFR slope was compared according to CKD stage, proteinuria category (microalbuminuria vs. overt proteinuria), and degree of tubular injury. 

The decline in eGFR  from 12 months prior to finerenone initiation (Δ0) to baseline was  decelerated by 24m monghts after the drug initiation (Δ1). Interestingly, the GFR slope slowed its declining rate significantly after 12 months of drug initiation (Δ2), indicating a flattening of the eGFR slope over time. This effect was particularly pronounced in patients with CKD stage 3 compared with those with stage 1-2 CKD. Finerenone significantly improved proteinuria, as reflected by reductions in UPCR and UACR. Urinary L-FABP and 2MG levels showed no significant deterioration after finerenone initiation. Subgroup analyses based on the degree of proteinuria or tubular injury revealed no significant differences in the changes in eGFR slope among groups.

Although finerenone did not clearly attenuate the eGFR decline within the first year of therapy, a slower eGFR slope was observed in the second year, suggesting a stabilization of renal function over time. The absence of worsening in tubular injury markers and sustained improvement in proteinuria indicate that finerenone may help preserve renal function and suppress CKD progression in patients with T2D. These findings support the potential long-term renoprotective effects of finerenone in real-world clinical practice.

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