MECHANISM OF KIDNEY DAMAGE IN GOUTY NEPHROPATHY

Abstract

Gout is a chronic metabolic disease caused by a disturbance in purine metabolism, characterized by the accumulation of sodium monourate (NMU) crystals in the joints, tophi, internal organs, and especially in the kidney tissues. These crystals act as the main trigger for initiating inflammatory processes in the body. Gouty nephropathy refers to various kidney damages associated with gout. This condition is not only related to the deposition of crystals but also closely linked to disruptions in purine metabolism, metabolic syndrome, hypertension, and vascular pathologies. The inflammatory effects of sodium monourate crystals are mediated through interleukin-1α (IL-1α), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), kinases (Syk, p38 MAPK), and inflammasomes. These processes play a significant role in the development of gouty nephropathy and cause severe damage to kidney tissues. This article analyzes the molecular basis, pathogenic mechanisms, and the impact of gouty nephropathy on kidney tissues as discussed in the existing literature.