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IgA肾病肾脏纤维化研究进展OA

Research progress of renal fibrosis in IgA nephropathy

中文摘要英文摘要

免疫球蛋白A(IgA)肾病(IgAN)以系膜区异常糖基化IgA1免疫复合物沉积为始动因素,通过激活补体及炎症反应触发细胞外基质重塑,形成肾小球硬化、间质纤维化、血管病变的纤维化进程.遗传易感性与黏膜免疫失衡、菌群失调、代谢紊乱协同作用,促进系膜细胞活化和足细胞损伤,构建促纤维化微环境.牛津分型中的肾小管萎缩/间质纤维化(T评分)是预测终末期肾病的关键组织学指标.当前诊断依赖肾活检,但非侵入性检测技术,如液体活检(微小RNA等)因高特异性和易获取性展现了潜力.治疗策略趋向多靶点联合干预,但受限于生物标志物验证不足和动态监测手段缺乏.未来需突破精准分型瓶颈,整合组学技术开发经组织验证的非侵入性标志物,构建基于分子分型的个体化治疗体系,实现纤维化进程的全程管控.

Immunoglobulin A(IgA)nephropathy(IgAN)initiated by abnormal glycosylated IgA1 im-mune complex deposition in mesangial region,which triggers extracellular matrix remodeling by activating complement and inflammatory reaction,thus forming the fibrosis process of glomerulosclerosis,interstitial fi-brosis and vascular disease.Genetic susceptibility cooperates with mucosal immune imbalance,flora imbalance and metabolic disorder to promote mesangial cell activation and podocyte damage,and build a fibrogenic mi-croenvironment.Tubular atrophy/interstitial fibrosis(T score)in the Oxford classification serves as a critical histological marker for predicting progression to end-stage renal disease.At present,the diagnosis depends on renal biopsy,but non-invasive detection techniques,such as liquid biopsy(MicroRNA,etc.),show potential because of their high specificity and accessibility.The treatment strategy tends to be multi-target combined in-tervention,but it is limited by the lack of biomarker verification and dynamic monitoring means.In the future,it is necessary to break through the bottleneck of accurate typing,integrate omics technology to develop non-invasive markers verified by tissues,build an individualized treatment system based on molecular subtyping and facilitate the full control of the fibrotic process.

宋佳蓉;李毅夫

中南大学湘雅二医院肾内科,湖南 长沙 410011中南大学湘雅二医院医学实验研究中心,湖南 长沙 410011

医药卫生

免疫球蛋白A肾病肾脏纤维化发病机制生物标志物治疗综述

Immunoglobulin A nephropathyRenal fibrosisPathogenesisBiomarkersThera-pyReview

《现代医药卫生》 2026 (1)

173-182,188,11

10.3969/j.issn.1009-5519.2026.01.033

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