Antifibrotic renal role of mineralcorticoid receptor antagonists

Abstract

Cardiovascular and renal diseases are one of the main health problems in all industrialized countries. Their incidence is constantly increasing due to the aging of the population and the greater prevalence of obesity and type 2 diabetes.

Clinical evidence suggests that aldosterone and the activation of mineralocorticoid receptors (MR) have a role in the pathophysiology of cardiovascular and renal diseases. Moreover, clinical studies demonstrate the benefits of mineralocorticoid receptor antagonists (MRAs) on mortality and progression of heart and kidney disease.

In addition to renal effects on body fluid homeostasis, aldosterone has multiple extrarenal effects including the induction of inflammation, vascular rigidity, collagen formation and stimulation of fibrosis.

Given the fundamental role of MR activation in renal and cardiac fibrosis, effective and selective blocking of the signal with MRAs can be used in the clinical practice to prevent or slow down the progression of heart and kidney diseases.

The aim of the present work is to review the role of MRAs in light of the new evidence as well as its potential use as an antifibrotic in chronic kidney disease (CKD). The initial clinical results suggest that MRAs are potentially useful in treating patients with chronic kidney disease, particularly in cases of diabetic nephropathy. We don’t yet have efficacy and safety data on the progression of kidney disease up to the end stage (ESRD) and filling this gap represents an important target for future trials.

 

Key words: mineralocorticoid receptor, aldosterone, kidney, cardiac, fibrosis

Sorry, this entry is only available in Italian.

Introduzione

L’aldosterone è un ormone steroideo con attività mineralcorticoide, prodotto principalmente nella zona glomerulare della corteccia surrenale. Le sue principali funzioni fisiologiche consistono nel mantenimento dell’equilibrio del sodio e del potassio e nel controllo della pressione arteriosa, legandosi ai recettori dei mineralcorticoidi (MR) nel tubulo distale e nel dotto collettore del rene e aumentando così il riassorbimento del sodio e la secrezione di potassio [1]. 

La visualizzazione dell’intero documento è riservata a Soci attivi, devi essere registrato e aver eseguito la Login con utente e password.