Kim Il Young, Lee Dong Won, Lee Soo Bong, Kwak Ihm Soo
Division of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of Korea ; Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 626-770, Republic of Korea.
Division of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of Korea ; Medical Research Institute, Pusan National University Hospital, Busan 602-739, Republic of Korea.
Biomed Res Int. 2014;2014:638732. doi: 10.1155/2014/638732. Epub 2014 May 5.
Hyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final common pathway in chronic kidney disease. Uric acid and xanthine oxidase may contribute to kidney fibrosis mainly by inducing inflammation, endothelial dysfunction, oxidative stress, and activation of the renin-angiotensin system. Besides, hyperuricemia induces alterations in renal hemodynamics via afferent arteriolopathy and contributes to the onset and progression of kidney fibrosis. Xanthine oxidase inhibitors may prevent kidney damage via lowering uric acid and/or inhibiting xanthine oxidase. However, there is still no sufficient evidence from interventional clinical researches supporting the causal relationship between uric acid and kidney fibrosis. The effect and role of xanthine oxidase inhibitors in preventing kidney fibrosis and chronic kidney disease progression must be further explored by performing future large scale clinical trials.
高尿酸血症是慢性肾脏病中常见的表现，原因是尿酸清除率降低。尿酸作为慢性肾脏病危险因素的作用一直存在很大争议，最近的研究表明尿酸在肾纤维化的发生和进展中起作用，肾纤维化是慢性肾脏病的最终共同途径。尿酸和黄嘌呤氧化酶可能主要通过诱导炎症、内皮功能障碍、氧化应激和肾素-血管紧张素系统激活而导致肾纤维化。此外，高尿酸血症通过入球小动脉病变引起肾血流动力学改变，并促进肾纤维化的发生和进展。黄嘌呤氧化酶抑制剂可能通过降低尿酸和/或抑制黄嘌呤氧化酶来预防肾脏损伤。然而，干预性临床研究仍没有足够证据支持尿酸与肾纤维化之间的因果关系。必须通过开展未来的大规模临床试验进一步探索黄嘌呤氧化酶抑制剂在预防肾纤维化和慢性肾脏病进展方面的效果和作用。
