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