ACTIVATION OF THE INTRARENAL RENIN-ANGIOTENSIN SYSTEM IN THE DEVELOPMENT OF GLOMERULOSCLEROSIS IN HYPERURICEMIA

Hyperuricemia is increasingly recognized as a major factor in the development of chronic kidney disease and glomerular injury. Elevated serum uric acid not only causes direct nephron damage but also activates the intrarenal renin-angiotensin system (RAS), leading to increased angiotensin II production. This activation elevates glomerular pressure, stimulates mesangial cell proliferation, and promotes extracellular matrix accumulation, resulting in progressive glomerulosclerosis. Oxidative stress, inflammatory cytokines, and fibrotic signaling pathways further exacerbate renal injury. Clinical and experimental evidence indicates that interventions targeting uric acid reduction and RAS inhibition can attenuate glomerular damage and slow the progression of kidney disease. Understanding the mechanisms linking hyperuricemia and intrarenal RAS activation is essential for the development of preventive and therapeutic strategies aimed at preserving renal function.