NLRP3 and Nephropathy: Renal medullary hypoxia and ischemia promote excessive ROS generation, which in turn triggers inflammatory pathways (e.g., activation of the NLRP3 inflammasome) and leads to tubular cell injury [14]. Oxidative stress not only precedes but actively contributes to functional and structural renal damage in the setting of contrast-induced nephropathy, establishing a central pathophysiologic role for ROS imbalance in disease evolution [15].