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高尿酸血症影响肾功能作用机制的研究进展
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Abstract:
人体血液中尿酸浓度过高会形成尿酸盐结晶(monosodium urate, MSU)，MSU在肾小管中沉积，导致肾间质和肾小管受损，引起痛风性肾病。此外，高尿酸可引起肾脏血流动力学改变、肾脏炎症反应和氧化应激等。多个信号通路参与了肾损伤过程，如：MAPK、Nrf2/ARE、NF-κB、PPAR等。高尿酸肾损伤可通过健康的生活方式预防，同时也需要规范化的药物治疗，但临床上降尿酸药物均存在一定的副作用，开发低毒高效的降尿酸药物具有重要的临床意义。本文综述了血尿酸水平升高引起肾损伤的机制，高尿酸血症的预防和治疗措施，为降尿酸保护肾脏的药物开发提供参考。
High uric acid concentration in human blood will form urate crystals (MSU), and MSU is deposited in renal tubules, leading to damage of renal interstitium and tubules and causing gouty nephropathy. In addition, high uric acid can cause alterations in renal hemodynamics as well as renal inflammatory response and oxidative stress. Signaling pathways associated with kidney injury include MAPK, Nrf2/ARE, NF-κB and PPAR. Hyperuric acid kidney injury can be prevented by a healthy lifestyle and also requires standardized drug therapy. However, all clinical uric acid-lowering drugs have certain side effects, and the development of safer and more effective uric acid-lowering drugs is urgent. This paper reviews the mechanism of kidney injury caused by elevated blood uric acid level, the prevention and treatment measures of hyperuricemia, and provides reference for the development of uric acid-lowering drugs to protect the kidneys.
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