# A retrospective cohort study on the impact of finerenone on the hepatic fibrosis indicator FIB-4

**Authors:** Bo An, Fang Chen, Wencheng An, Zhijun Cui, Lin Jiang, Shujing Zhou, Mingda Song, Wei Huang, Huixian Yan

PMC · DOI: 10.3389/fendo.2026.1745102 · Frontiers in Endocrinology · 2026-02-10

## TL;DR

This study examines how finerenone affects liver fibrosis in patients with diabetes and kidney disease, finding a slight decrease in a fibrosis marker over time.

## Contribution

The study provides real-world evidence of finerenone's potential impact on hepatic fibrosis in T2DM patients with CKD.

## Key findings

- Finerenone showed a trend toward lowering FIB-4 values in patients with T2DM and CKD.
- Longer treatment duration was associated with a greater reduction in FIB-4.
- No treatment discontinuations due to hyperkalemia were observed.

## Abstract

This study aimed to evaluate the influence of finerenone, a novel nonsteroidal selective mineralocorticoid receptor antagonist (nsMRA), on the hepatic fibrosis indicator FIB-4, as well as its safety profile in hospitalized patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) managed in the endocrinology department.

A single-center, retrospective cohort design was employed, enrolling 138 consecutive hospitalized patients who initiated finerenone therapy for the first time in our endocrinology department between June 2023 and December 2024. Baseline data and subsequent outpatient follow-up records were extracted to calculate the FIB-4 and assess changes in hepatic and renal function, serum potassium levels, and adverse events during treatment.

Of the enrolled cohort, 119 patients (85.6%) had complete baseline laboratory profiles, with a mean age of 63.1 years and 58% male. Baseline FIB-4 median 1.15. Among 52 patients (43%) who completed follow-up, the median follow-up duration was 6 months (range 1–16 months). The median follow-up FIB-4 declined to 1.10, representing an absolute reduction of 0.05. Patients with follow-up exceeding 12 months follow-up showed a further reduction to 0.96. Importantly, no cases of treatment discontinuation due to hyperkalemia were documented during follow-up.

In real-world clinical practice, finerenone in T2DM patients with CKD trended to lower FIB-4 values, especially with longer use. However, no statistical significance and study limitations preclude definitive conclusions on its antifibrotic activity. These findings are hypothesis-generating and need confirmation in large, prospective, long-term studies with robust endpoints and proper controls.

## Linked entities

- **Chemicals:** finerenone (PubChem CID 24993045)
- **Diseases:** type 2 diabetes mellitus (MONDO:0005148), chronic kidney disease (MONDO:0005300)

## Full-text entities

- **Genes:** GGTLC4P (gamma-glutamyltransferase light chain 4 pseudogene) [NCBI Gene 729838] {aka GGT}, CCN2 (cellular communication network factor 2) [NCBI Gene 1490] {aka CTGF, HCS24, IBP-8, IGFBP8, KMD, NOV2}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, COL1A1 (collagen type I alpha 1 chain) [NCBI Gene 1277] {aka CAFYD, EDSARTH1, EDSC, OI1, OI2, OI3}, NR3C2 (nuclear receptor subfamily 3 group C member 2) [NCBI Gene 4306] {aka MCR, MLR, MR, NR3C2VIT}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, SGK1 (serum/glucocorticoid regulated kinase 1) [NCBI Gene 6446] {aka SGK}
- **Diseases:** renal failure (MESH:D051437), NAFLD (MESH:D065626), Hepatic fibrosis (MESH:D008103), CKD (MESH:D051436), hepatitis B (MESH:D006509), inflammation (MESH:D007249), Liver Diseases (MESH:D008107), cirrhosis (MESH:D005355), Hyperglycemia (MESH:D006943), metabolic syndrome (MESH:D024821), Hyperkalemia (MESH:D006947), hypotensive syncope (MESH:D007022), fatty liver disease (MESH:D005234), gynecomastia (MESH:D006177), AKI (MESH:D058186), insulin resistance (MESH:D007333), hepatitis C virus (HCV) infection (MESH:D006526), acute-on-chronic liver failure (MESH:D065290), breast tenderness (MESH:D061325), death (MESH:D003643), HCC (MESH:D006528), autoimmune hepatitis (MESH:D019693), T2DM (MESH:D003924), heart failure (MESH:D006333), drug-induced liver injury (MESH:D056486), hyperaldosteronism (MESH:D006929), liver disorder (MESH:D017093)
- **Chemicals:** carbon tetrachloride (MESH:D002251), aldosterone (MESH:D000450), nsMRA (-), potassium (MESH:D011188), alcohol (MESH:D000438), Finerenone (MESH:C576501), spironolactone (MESH:D013148)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

19 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929166/full.md

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Source: https://tomesphere.com/paper/PMC12929166