Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, China.
Biomed Res Int. 2020 Jun 26;2020:5817348. doi: 10.1155/2020/5817348. eCollection 2020.
Uric acid is the end product of purine metabolism in humans, and its excessive accumulation leads to hyperuricemia and urate crystal deposition in tissues including joints and kidneys. Hyperuricemia is considered an independent risk factor for cardiovascular and renal diseases. Although the symptoms of hyperuricemia-induced renal injury have long been known, the pathophysiological molecular mechanisms are not completely understood. In this review, we focus on the research advances in the mechanisms of hyperuricemia-caused renal injury, primarily on oxidative stress, endothelial dysfunction, renal fibrosis, and inflammation. Furthermore, we discuss the progress in hyperuricemia management.
尿酸是人类嘌呤代谢的终产物，其在体内的过度积累会导致高尿酸血症和尿酸盐晶体在关节和肾脏等组织中的沉积。高尿酸血症被认为是心血管和肾脏疾病的独立危险因素。尽管高尿酸血症引起的肾损伤的症状早已为人所知，但病理生理分子机制尚未完全阐明。在这篇综述中，我们重点介绍了高尿酸血症引起肾损伤的机制的研究进展，主要涉及氧化应激、内皮功能障碍、肾纤维化和炎症。此外，我们还讨论了高尿酸血症管理的进展。
