截至目前,有关IgA肾病(IgAN)的发病机制尚不完全清楚,但近年来相关研究已取得了明显的进展。研究提示异常糖基化IgA1免疫复合物及后续的免疫反应可导致IgAN的进展,清除系膜区IgA1可能成为治疗IgAN的新靶向;另有研究发现全身性氧化应激能增强IgAN异常糖基化IgA的肾毒性。氧化剂不仅与小管间质的损伤有关,还与疾病的进展有关,也与肾小球的初期损伤有关;也有研究显示先天免疫的失常可导致黏膜抗原消除失败、IgA合成改变及炎性反应,可能与IgAN发生和进展有密切的关系。现就有关研究进展进行综述。 Up to now, the pathogenesis of IgA nephropathy (IgAN) is not yet fully understood, but the relevant research has made significant progress in recent years. Studies suggest that abnormal glycation of IgA1 immune complexes and follow-up of immune response can lead to the progress of IgAN, clear mesangial IgA1 may be a new target for the treatment of IgAN; another study found that systemic oxidative stress can increase IgAN abnormal glycosylation IgA nephrotoxicity. Oxidants are not only associated with tubulointerstitial damage, but also with the progress of the disease, but also with the initial glomerular injury; also studies have shown that abnormalities in innate immunity can lead to the elimination of mucosal antigen failure, IgA synthesis and inflammatory reactions may change And IgAN occurrence and progress are closely related. Now on the progress of the review.