中文摘要：

目的探讨IgA肾病（IgAN）患者肾组织分泌型IgA（sIgA）的沉积与其临床、病理及补体激活的关系。方法收集肾活检确诊的原发性IgAN患者，免疫比浊及ELISA法检测患者血清中补体的激活，免疫荧光激光共聚焦显微镜检测肾组织中sI外的沉积及补体的激活，分析sIgA的沉积与患者临床、病理及补体激活的关系。结果201例患者中，59例患者肾脏有sIgA的沉积。与无沉积的患者相比，SIgA沉积的患者肉眼血尿及黏膜感染发生率高（P〈0．05），血清胱抑素c及B2微球蛋白、肾小管间质病变程度及牛津评分的T评分均较低（P〈0．05）；对其中107例患者进行补体检测发现，伴或不伴SIgA沉积的患者，血清及肾组织中补体激活的差异无统计学意义（P〉O．05），但与旁路途径激活的患者相比，肾组织甘露糖结合凝集素（MBL）途径激活的患者eGFR较低（P〈0．01），血肌酐、肾小球硬化比例、牛津评分的s评分以及肾小管间质的损伤程度均较高（P〈0．05）。结论SIgA沉积的IgAN患者与黏膜免疫关系更密切；与无SIgA沉积的患者相比，SIgA沉积患者部分临床及病理特点不同但补体激活情况相似，而MBL途径激活的患者。肾脏损伤更重。

英文摘要：

Objective To further investigate the association among clinical pathology, complement activation and renal secretory IgA （SIgA） deposition in patients with IgA nephropathy （IgAN）. Methods The activation of serum complements were detected by immunoturbidimetry and ELISA. Renal deposition of SIgA and activation of complements were detected by immunofluorescence. Then the association among clinical pathology, complement activation and renal SIgA deposition were analyzed in IgAN patients. Results In all 201 patients with IgAN, 59 patients had SIgA deposition with higher incidences of mucosal infection history and hematuria （P 〈 0.05）, lower levels of serum cystatin C, 132 microglobulin and lower tubulointerstitial lesion grades and T- grade in the Oxford classification （P 〈 0.05）, when compared with patients without SIgA deposition. Both alternative and mannose binding lectin （MBL） pathways were activated in patients with or without SIgA deposition. Patients with MBL pathway activation had lower estimate glomerular filtration rate （P 〈 0.01）, higher serum creatinine, higher proportion of glomerulosclerosis and S-grade in the Oxford classification, more severe tubulointerstitial lesion （P 〈 0.05）. Conclusions Compared with patients without SIgA deposition, patients with SIgA deposition have a stronger link to mucosal immune. The deposition of SIgA is associated with different clinical and pathological manifestations; however, the complement activation is similar in both groups of patients. Patients with MBL pathway activation show more severe kidney injury.