摘要：高尿酸血症肾病是由高尿酸血症引起的早期隐匿和持续进展的继发性肾脏损伤。最近研究表明，血管生成素样蛋白3(ANGPTL3)对血管内皮表面的在足细胞表达的整合素β3(avβ3)具有强大的激活功能，从而引起肾小球足细胞通透性升高，出现蛋白尿及肾脏损害，现将ANGPTL3在高尿酸血症肾病发病机制的研究进展进行阐述，以期为高尿酸血症肾病的临床治疗提供参考。

    关键词：血管生成素样蛋白3；高尿酸血症肾病；肾损害发病机制；足细胞

    中图分类号：R259" " " " " " " " " " " " " " " " " "文献标识码：A" " " " " " " " " " " " " " " " "DOI：10.3969/j.issn.1006-1959.2025.03.036

    文章编号：1006-1959(2025)03-0175-04

    Research Progress of Angiopoietin-like Protein 3 in the Pathogenesis of Hyperuricemic Nephropathy

    GUO Lijiang， YANG Xiaorong， JI Yingying， XU Lijie， ZHOU Shuhong

    (First School of Clinical Medical， Gansu University of Chinese Medicine， Lanzhou 730000， Gansu， China)

    Abstract：Hyperuricemic nephropathy is an early occult and progressive secondary renal injury caused by hyperuricemia. Recent studies have shown that angiopoietin-like protein 3 (ANGPTL3) has a strong activation function on the expression of integrin β3 (avβ3) on the surface of vascular endothelium， which leads to the increase of glomerular podocyte permeability， proteinuria and renal damage. This article reviews the research progress of ANGPTL3 in the pathogenesis of hyperuricemic nephropathy ......