# Finerenone in mildly reduced or preserved ejection fraction and chronic kidney disease: a narrative review

**Authors:** Muhammad Shaheer Bin Faheem, Hafiza Qurat Ul Ain, Aatka Rauf, Qasra Faheem, Own E Mohammad Najmi

PMC · DOI: 10.1186/s43044-026-00722-x · The Egyptian Heart Journal · 2026-03-01

## TL;DR

Finerenone, a non-steroidal drug, shows promise in treating heart failure and kidney disease in type 2 diabetes patients with fewer side effects.

## Contribution

The paper highlights finerenone's novel efficacy and safety in managing heart failure with preserved ejection fraction and chronic kidney disease.

## Key findings

- Finerenone reduces hospitalizations and cardiovascular risks in heart failure patients.
- It has fewer side effects compared to traditional steroidal MRAs.
- Clinical trials show it slows kidney disease progression in type 2 diabetes patients.

## Abstract

In patients with type 2 diabetes and chronic kidney disease (CKD) heart failure with preserved ejection fraction is associated with considerable morbidity and it has fewer treatment options available. HFpEF, which is characterized by increased cardiovascular risks and poor outcomes, continues to be a therapeutic challenge, particularly in older persons.

A non-steroidal mineralocorticoid receptor antagonist (MRA), finerenone has excellent therapeutic potential in patients with HFpEF and CKD, notably those with diabetes type 2. Research indicate that Finerenone preferentially targets mineralocorticoid receptors associated with inflammation and fibrosis and that it also has an advantage over commonly used steroidal MRAs (e.g., spironolactone), which carry significant risks such as hyperkalemia, gynecomastia, and renal impairment. There are two phase 3 clinical trials namely FIDELIO-DKD and FIGARO-DKD demonstrating how effectively finerenone works in preventing the progression of renal damage and cardiovascular events in type 2 diabetic patients and in patients with CKD. In addition, the FINEARTS-HF study shows that hospitalizations for heart failure were reduced with use of finerenone and also the overall decline in individuals with HFpEF across all ages, particularly the older populations. Finally, Finerenone is found to be more appropriate for patients with complex medical histories because its safety profile shows fewer side effects compared to the traditional steroidal MRAs, as it has lower risks for electrolyte imbalances and renal function deterioration.

This article addresses the safety, efficacy, mechanism of action, and various trials conducted on Finerenone and how it gained importance as an effective substitute in the management of HFpEF and CKD, decreasing morbidity and mortality risks while limiting adverse effects.

## Linked entities

- **Chemicals:** Finerenone (PubChem CID 24993045), spironolactone (PubChem CID 5833)
- **Diseases:** type 2 diabetes (MONDO:0005148), chronic kidney disease (MONDO:0005300)

## Full-text entities

- **Genes:** NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, 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}
- **Diseases:** inflammation (MESH:D007249), fibrosis (MESH:D005355), hyperkalemia (MESH:D006947), dyspnea (MESH:D004417), diabetes (MESH:D003920), cardiac working abnormalities (MESH:D000073397), CKD (MESH:D051436), gynecomastia (MESH:D006177), obesity (MESH:D009765), fatigue (MESH:D005221), stroke (MESH:D020521), deterioration of renal function (MESH:D058186), renal (MESH:D006030), hypotension (MESH:D007022), proteinuria (MESH:D011507), Reduced kidney function (MESH:D007680), iron deficiency (MESH:D000090463), Co (MESH:D060085), cardio (MESH:D059347), anemia (MESH:D000740), albuminuria (MESH:D000419), hypertension (MESH:D006973), Cardiovascular diseases (MESH:D002318), uremic toxins (MESH:D006463), myocardial infarction (MESH:D009203), T2D (MESH:D003924), Renal disease (MESH:D007674), HF (MESH:D006333), peripheral and pulmonary oedema (MESH:D010523), cardiac hypertrophy (MESH:D006332), cardiac incidents (MESH:D006331), CAD (MESH:D003324), type two diabetes (MESH:D003922), diabetic kidney disease (MESH:D003928), necrosis (MESH:D009336), HFpEF (MESH:D054144)
- **Chemicals:** salt (MESH:D012492), Nitrogen (MESH:D009584), carbon-14 (MESH:C000615234), aldosterone (MESH:D000450), [C (MESH:D002244), eplerenone (MESH:D000077545), ACEi (-), potassium (MESH:D011188), natriuretic peptides (MESH:D045265), deoxycorticosterone acetate (MESH:D064791), Urea (MESH:D014508), spironolactone (MESH:D013148), creatinine (MESH:D003404), Finerenone (MESH:C576501), ROS (MESH:D017382)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12950832/full.md

## References

5 references — full list in the complete paper: https://tomesphere.com/paper/PMC12950832/full.md

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Source: https://tomesphere.com/paper/PMC12950832