Protected: Effects of Finerenone on proteinuria and progression of chronic kidney disease

Abstract

A growing body of experimental and clinical evidence confirms that aldosterone contributes, independently from its classical homeostatic effects, to the pathogenesis and progression of chronic kidney disease (CKD).
In fact, the activation of the mineralocorticoid receptor (MR) in the kidney, present at the podocyte, mesangial, endothelial as well as at the tubulointerstitial levels, has been linked to podocyte damage and consequent apoptosis, proliferation of mesangial cells, inflammation of the tubulointerstitial compartment and, more generally, to the final outcome of interstitial fibrosis and glomerular sclerosis.
Therefore, blockade of the MR may represent an effective treatment of CKD.
Today, within the class of mineralocorticoid receptor antagonists (MRA), several molecules are available, with different pharmacokinetic and pharmacodynamic characteristics. In this brief review we will focus on the characteristics of these molecules and in particular on Finerenone, a new generation, non-steroidal MRA, characterized by minimal side effects and high pharmacological efficacy.

Keywords: mineralcorticoid receptor antagonists; chronic kidney disease; hyperkalemia; cardiovascular risk; finerenone.

This content is password protected. To view it please enter your password below: