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Published in: Current Cardiology Reports 10/2022

04-08-2022 | Eplerenon | Hypertension (DS Geller and DL Cohen, Section Editors)

Effects of Finerenone, a Novel Nonsteroidal Mineralocorticoid Receptor Antagonist, on Cardiovascular Disease, Chronic Kidney Disease, and Blood Pressure

Authors: Jonathan D. Ravid, Luke J. Laffin

Published in: Current Cardiology Reports | Issue 10/2022

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Abstract

Purpose of Review

Finerenone, an FDA-approved nonsteroidal mineralocorticoid receptor (MR) antagonist, has been evaluated in context of chronic kidney disease (CKD) and associated cardiovascular disease (CVD). In this review, we summarize pre-clinical and clinical studies focused on the impact of finerenone on these disease processes.

Recent Findings

Activation of the MR upregulates genes encoding for facilitators of tissue damage. Finerenone binding to a helix domain in this receptor inhibits receptor function. Studies in murine models of kidney disease, heart failure, hypertension, and vascular injury demonstrate significant protective effects of finerenone against further disease progression, as well as association with reduced oxidative stress, inflammation, and fibrosis. Phase 1–3 clinical trials with finerenone show safety and efficacy in improving renal and cardiovascular outcomes in patients with CKD.

Summary

Research thus far encourages the addition of finerenone to the standard of care for certain CKD patients, especially those especially at risk for or with pre-existing cardiovascular disease. Continued study of the effect of finerenone in diverse patient populations and different disease states is needed.
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Metadata
Title
Effects of Finerenone, a Novel Nonsteroidal Mineralocorticoid Receptor Antagonist, on Cardiovascular Disease, Chronic Kidney Disease, and Blood Pressure
Authors
Jonathan D. Ravid
Luke J. Laffin
Publication date
04-08-2022
Publisher
Springer US
Published in
Current Cardiology Reports / Issue 10/2022
Print ISSN: 1523-3782
Electronic ISSN: 1534-3170
DOI
https://doi.org/10.1007/s11886-022-01750-0

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