MECHANISMS OF KIDNEY INJURY WITH ELEVATED URIC ACID: INFLAMMATION, OXIDATIVE STRESS, ENDOTHELIAL DYSFUNCTION

Hyperuricemia has emerged as an important factor in the progression of chronic kidney disease. Elevated levels of uric acid contribute to renal injury through mechanisms including inflammation, oxidative stress, and endothelial dysfunction. Inflammatory processes trigger cytokine production and immune cell recruitment, leading to glomerular and tubular damage. Oxidative stress damages renal cells and amplifies pro-inflammatory signaling, while endothelial dysfunction impairs renal microcirculation and increases blood pressure, further accelerating kidney injury. Clinical and experimental evidence indicates that early identification and effective management of hyperuricemia, through lifestyle modification and pharmacological therapy, can slow the decline of kidney function and improve patient outcomes. Understanding the interplay of these mechanisms is critical for developing targeted therapeutic strategies in patients with elevated uric acid.