PATHOPHYSIOLOGICAL MECHANISMS UNDERLYING RENAL PARENCHYMAL INJURY IN HYDRONEPHROSIS

Abstract

Hydronephrosis is a pathological condition characterized by dilation of the renal collecting system and progressive injury to the renal parenchyma as a consequence of urinary tract obstruction. The development and progression of hydronephrosis involve a complex interplay of increased intrarenal pressure, hemodynamic disturbances, tissue hypoxia, oxidative stress, inflammatory responses, and fibrotic remodeling. The severity and duration of urinary tract obstruction determine the extent of structural and functional alterations within the renal parenchyma. At the molecular level, activation of the renin–angiotensin–aldosterone system (RAAS), TGF-β1/Smad signaling, NF-κB-mediated inflammatory pathways, and mitochondrial dysfunction play crucial roles in disease progression. This study analyzes the principal pathophysiological and molecular mechanisms underlying renal parenchymal injury in hydronephrosis. A comprehensive understanding of these mechanisms may facilitate the development of novel therapeutic strategies aimed at preventing irreversible loss of renal function.