# Effect of finerenone on renal function in patients with type 2 diabetic nephropathy: a retrospective cohort study

**Authors:** Xu-Ying Liu, Ya-Min Zhao, Ya-Guang Zhang, Yi Liu, Bo-Ya Wang, Zhen-Zhen Hao, Man-Hui Hu

PMC · DOI: 10.3389/fendo.2026.1753126 · Frontiers in Endocrinology · 2026-02-10

## TL;DR

Adding finerenone to standard therapy improved kidney function in patients with type 2 diabetic nephropathy over 24 weeks.

## Contribution

This study shows that finerenone, when added to ACEI/ARB therapy, reduces the risk of kidney function decline in diabetic nephropathy patients.

## Key findings

- Patients on finerenone had significantly better eGFR and lower UACR compared to controls after 24 weeks.
- Finerenone treatment independently protected against a ≥15% eGFR decline.
- Both treatment groups were well tolerated with no increase in serious adverse events.

## Abstract

Diabetic nephropathy (DN) remains a major cause of chronic kidney disease despite optimized renin–angiotensin system blockade. This study aimed to evaluate the efficacy and safety of adding finerenone to angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker (ACEI/ARB) therapy and to identify predictors of clinically meaningful renal deterioration in patients with DN.

This retrospective cohort study enrolled adult patients (18–80 years) with a confirmed diagnosis of DN according to American Diabetes Association and Kidney Disease: Improving Global Outcomes criteria, who had complete baseline and follow-up data. Patients with type 1 diabetes, non-diabetic kidney disease, severe hepatic dysfunction, advanced heart failure, recent acute cardiovascular events, or baseline hyperkalemia were excluded. A total of 240 patients treated between January 2019 and December 2024 were included. Patients receiving ACEI/ARB monotherapy (control group, n = 124) were compared with those receiving ACEI/ARB plus finerenone (observation group, n = 116). Renal and metabolic parameters were assessed at baseline and after 24 weeks. Between-group comparisons were performed using appropriate parametric or nonparametric tests, and multivariable logistic regression analysis was conducted to identify independent predictors of a ≥15% estimated glomerular filtration rate (eGFR) decline.

After 24 weeks, patients receiving finerenone showed significantly lower Scr (128.3 ± 27.6 μmol/L vs. 140.8 ± 35.1 μmol/L, P = 0.002), higher eGFR (56.8 ± 11.4 vs. 50.1 ± 12.3 mL/min/1.73 m², P < 0.001), and lower UACR (301.4 ± 142.7 vs. 398.7 ± 176.8 mg/g, P < 0.001) than controls. Finerenone treatment independently protected against renal deterioration (adjusted odds ratio [aOR] = 0.473, 95% CI: 0.253–0.883, P = 0.019), while longer diabetes duration, lower baseline eGFR, and higher UACR predicted ≥15% eGFR decline. Both regimens were well tolerated, with no increase in severe hyperkalemia or serious adverse events.

Adding finerenone to ACEI/ARB therapy improved renal parameters over 24 weeks and was independently associated with reduced risk of clinically meaningful eGFR decline without excess serious adverse events.

## Linked entities

- **Chemicals:** finerenone (PubChem CID 24993045)
- **Diseases:** chronic kidney disease (MONDO:0005300), diabetes (MONDO:0005015), heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, RRAS (RAS related) [NCBI Gene 6237] {aka R-Ras, RRAS1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, NR3C2 (nuclear receptor subfamily 3 group C member 2) [NCBI Gene 4306] {aka MCR, MLR, MR, NR3C2VIT}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}
- **Diseases:** proteinuria (MESH:D011507), hypotension (MESH:D007022), renal (MESH:D006030), acute kidney injury (MESH:D058186), fatigue (MESH:D005221), function (MESH:D003291), Diabetes (MESH:D003920), renal function decline (MESH:D060825), Reduced renal function (MESH:D001523), CKD (MESH:D051436), fibrosis (MESH:D005355), Hyperlipidemia (MESH:D006949), hyperglycemia (MESH:D006943), hepatic dysfunction (MESH:D008107), inflammatory (MESH:D007249), nephrotic (MESH:D009404), Hyperkalemia (MESH:D006947), hematuria (MESH:D006417), Diabetic nephropathy (MESH:D003928), hyperuricemia (MESH:D033461), heart failure (MESH:D006333), Kidney Disease (MESH:D007674), T2D (MESH:D003924), type 1 diabetes (MESH:D003922), gastrointestinal discomfort (MESH:D005767), end-stage renal disease (MESH:D007676), diabetic retinopathy (MESH:D003930), endocrine or metabolic disorders (MESH:D004700), dizziness (MESH:D004244), reduction (MESH:D015431), albuminuria (MESH:D000419), Hypertension (MESH:D006973), III (MESH:C537189)
- **Chemicals:** Finerenone (MESH:C576501), glucose (MESH:D005947), creatinine (MESH:D003404), spironolactone (MESH:D013148), ACEI (-), K (MESH:D011188)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

31 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929165/full.md

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Source: https://tomesphere.com/paper/PMC12929165