There is compelling evidence supporting the renin-angiotensin-aldosterone system contribution in experimental and human renal disease. Interruption of this system by converting enzyme inhibition or angiotensin II receptor antagonism reduces injury. Angiotensin II contributes to the progression of renal disease through its direct vascular effects and proliferative properties. The mediators of angiotensin II induced renal injury are many and include TGF-beta, PDGF, bFGF, and endothelin. Though the mechanisms involved in its contribution to progressive renal disease are not well delineated, aldosterone seems to be an overlooked contributor to the progression of kidney disease and its effects may also depend on both its hemodynamic and more direct cellular actions.