The paradox of the renin-angiotensin system in chronic renal disease.

Abstract

Despite normal to suppressed levels of renin activity in chronic renal disease, multiple lines of evidence suggest a role for the RAS, especially its intrarenal expression, in several critical aspects of this condition. Alterations in the distribution and control of components of the renal RAS could account for localized areas of activation of this system. Renal scarring may be particularly important as a major stimulus to renin synthesis in the diseased kidney. While both intrarenal and systemic hypertension may depend in part upon actions of the RAS, other non-hemodynamic actions of the RAS may also contribute to the adaptation of residual nephrons as well as their progressive injury.