ScholarWorks@중앙대학교

초록

Hyperuricemia is frequently observed in patients with chronic kidney disease and is recognized as a significant contributor to the progression of renal dysfunction. On the other hand, hypouricemia, although less thoroughly studied, has been implicated in exercise-induced acute kidney injury and urolithiasis. Uric acid (UA), the final product of purine metabolism, is predominantly synthesized in the liver and excreted through both renal and intestinal pathways. The metabolism and excretion of UA are intricately linked to kidney function, underscoring their clinical significance in the context of renal disease. This review provides a comprehensive review of UA metabolism and the key urate transporters, including URAT1, GLUT9, OATs, and ABCG2, which play pivotal roles in maintaining UA homeostasis. Additionally, this review discusses the genetic and environmental factors that influence UA regulation, with a particular focus on the pathological consequences of transporter dysfunction. By elucidating the mechanisms underlying UA handling in the renal and intestinal systems, this review aims to enhance our understanding of UA-related pathophysiology, and to inform the development of targeted therapeutic strategies for modulating UA transport.

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