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.
Bibliographical noteFunding Information:
This review is a revision of a published article (in Contemporary Issues in Nephrology: The Progressive Nature of Renal Disease, edited by MITCH WE, New York, Churchill Livingstone, 26:55—76, 1992). This work was supported by US Public Health Service Grants AM-3 1437 (T.H.H.) and R29DK43075 (M.E.R.), and by a Young Investigator Grant from the National Kidney Foundation (M.E.R.). Dr. Correa-Rotter was a recipient of Juvenile Diabetes Foundation International
Postdoctoral Research Fellowship, and was also partially supported by the Instituto Nacional de Ia NutriciOn Salvador Zubirán, Mexico City.