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Non-steroidal mineralocorticoid receptor antagonism for the treatment of cardiovascular and renal disease
Pharmaceutical antagonism of the mineralocorticoid receptor (MR) can protect against organ damage caused by elevated aldosterone levels in patients experiencing heart failure (HF), chronic kidney disease (CKD), primary aldosteronism, and hypertension. While traditional steroid‐based MR antagonists e...
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Published in: | European journal of heart failure 2016-01, Vol.18 (1), p.28-37 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Pharmaceutical antagonism of the mineralocorticoid receptor (MR) can protect against organ damage caused by elevated aldosterone levels in patients experiencing heart failure (HF), chronic kidney disease (CKD), primary aldosteronism, and hypertension. While traditional steroid‐based MR antagonists effectively reduce mortality rates and extend patient survival, their broad application has been limited by significant side effects, most notably hyperkalaemia. Recently, finerenone (BAY 94‐8862) has emerged as a next‐generation non‐steroidal dihydropyridine‐based MR antagonist designed to minimize off‐target effects while maintaining potent efficacy. In this review, the outcomes of finerenone therapy in several diseases associated with MR activity are explored. The (pre‐) clinical efficacy of finerenone is compared with that of traditional steroid‐based MR antagonists. Finally, recent and ongoing clinical trials using finerenone to treat chronic HF, CKD, and diabetic nephropathy are discussed. Taken together, pre‐clinical and clinical evidence suggests that finerenone may achieve equivalent organ‐protective effects with reduced levels of electrolyte disturbance compared with traditional steroid‐based MR antagonists. This supports further clinical development of finerenone for the treatment of cardiovascular and renal disease. |
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ISSN: | 1388-9842 1879-0844 |
DOI: | 10.1002/ejhf.444 |