A CLINICAL APPROACH IN REGRESSION OF GLOMERULOSCLEROSIS

Abstract

The role of the renin angiotensin System (RAS) in hypertension and end organ damage has long been recognized. Recent advances in genetic models and newly available pharmacological tools have allowed dissection of the mechanisms of actions of the components of the RAS in fibrotic kidney disease. Numerous studies have shown that angiotensin l converting enzyme inhibitors (ACEI) are superior to other antihypertensive agents in protecting the kidney against progressive deterioration, even in normotensive persons2,3. Like ACEI, angiotensin II type 1 receptor antagonists (AT1RA) ameliorate or even reverse glomerulosclerosis in rat animal models. These findings suggest that angiotensin II. The beneficial effect on renal fibrosis of inhibiting the RAS likely reflects the central role that angiotensin has in regulating renal function and structure by its various actions. This article explores the interaction of the renin angiotensin aldosterone System with PAI-1, and the potential significance of these interactions in the pathogenesis of progressive renal disease and remodeling of renal sclerosis.