Purpose of review
Current evidence showcases the pathologic effects of excess aldosterone
in promoting glomerular and tubulointerstitial inflammation and fibrosis through various pathways. The place for mineralocorticoid receptor antagonists
(MRAs) in chronic kidney disease
(CKD) progression is unclear.
MRAs further reduce albuminuria and blood pressure in CKD patients when used in conjunction with angiotensin-converting enzyme inhibitor or angiotensin receptor blockers. The usage of MRAs as disease-modifying therapy in CKD patients has been hampered by concern over worsening kidney function and hyperkalemia
. Recent data from small studies highlight a way that these agents may be used with no fear of hyperkalemia
. Additionally, they have been shown to further lower blood pressure and albuminuria when hyperkalemia
is no longer a safety issue. Additionally, novel MRAs are in phase 3 clinical trials and these are discussed.
MRAs have a clear role in further reducing very high albuminuria when used with other renin–angiotensin system blockers; however, hyperkalemia
is a limiting factor for the use of MRAs. Use of the new potassium binder patiromer has facilitated the use of MRAs in CKD, and novel nonsteroidal MRAs are currently being tested in advanced CKD outcome trials.