THE ROLE OF RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM ACTIVATION IN THE PATHOGENESIS OF OBSTRUCTIVE UROPATHY

Abstract

Obstructive uropathy is a pathological condition characterized by partial or complete impairment of urinary flow, leading to progressive deterioration of renal function. Altered intrarenal hemodynamics, tissue hypoxia, oxidative stress, and inflammatory responses play critical roles in the pathogenesis of this condition. In recent years, activation of the renin–angiotensin–aldosterone system (RAAS) has been recognized as one of the central molecular mechanisms involved in the development of obstructive nephropathy. Through increased concentrations of angiotensin II and aldosterone, RAAS activation promotes vasoconstriction, inflammation, oxidative stress, and fibrogenesis. These alterations contribute to the development of tubulointerstitial fibrosis and chronic kidney disease. This study analyzes the molecular and cellular significance of RAAS activation in obstructive uropathy. Therapeutic strategies targeting components of the RAAS represent a promising approach for slowing the progression of obstructive nephropathy.