首页|高尿酸血症致肾小管损伤机制的研究进展

高尿酸血症致肾小管损伤机制的研究进展

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尿酸是人体嘌呤代谢的最终产物.当尿酸生成过多或排泄减少时,尿酸在体内过度积累可导致高尿酸血症.高尿酸血症被认为是肾脏损伤和慢性肾脏病的独立危险因素.当尿酸浓度超过正常生理范围时可引起肾小管的多种病理反应,但其病理生理机制尚不完全清楚.本文就高尿酸血症导致肾小管损伤的分子机制进行综述,包括高尿酸血症中尿酸诱导的自噬、炎症、氧化应激、凋亡、上皮-间充质转化和纤维化等过程.
Research progress on the mechanism of renal tubular injury caused by hyperuricemia
Uric acid is the final product of purine metabolism in the human body.When uric acid is produced too much or excreted is reduced,excessive accumulation of uric acid in the body can lead to hyperuricemia.Hyperuricemia is considered to be an independent risk factor for kidney damage and chronic kidney disease.When the concentration of uric acid exceeds the normal physiological range,it can cause a variety of pathological reactions in the renal tubules,but its pathophysiological mechanism is not fully understood.This article reviews the molecular mechanisms of renal tubular damage caused by hyperuricemia,including autophagy,inflammation,oxidative stress,apoptosis,epithelial-mesenchymal transition,fibrosis,and other processes induced by uric acid in hyperuricemia.

HyperuricemiaRenal tubule injuryUric acidMechanism

许颖、徐思宇、王传旭、邵命海

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上海中医药大学附属曙光医院肾病科,上海 201203

上海中医药大学中医肾病研究所,上海 201203

高尿酸血症 肾小管损伤 尿酸 机制

2024

中国医药导报
中国医学科学院

中国医药导报

CSTPCD
影响因子:1.759
ISSN:1673-7210
年,卷(期):2024.21(22)