Experimental evidence indicates that aldosterone, besides its mineralcorticoid properties, directly contributes to accelerate renal damage through promotion of cell growth, fibrosis and inflammation. As a consequence, attenuation of growth-promoting and fibroproliferative effects of aldosterone might contribute to slow progression of chronic renal injury. Preliminary clinical observations have documented that aldosterone blockers added to angiotensin-converting enzyme inhibitor- and/or angiotensin receptor blocker-based regimens exerted significant antiproteinuric effects in patients with diabetic and nondiabetic nephropathies. Further studies in larger cohorts are now required to definitively address the safety and efficacy of aldosterone antagonism in patients with chronic kidney diseases.