中国血液净化

中国血液净化

• 基础研究 • 上一篇    下一篇

伴IgA沉积的微小病变肾病综合征患者血清IgA1糖基化缺陷的检测

  

  1. 北京大学人民医院肾内科
  • 收稿日期:2012-07-15 出版日期:2012-10-12 发布日期:2013-01-04
  • 通讯作者: 王梅
  • 基金资助:

    国家自然科学基金青年科学基金项目（项目号：81000296）
     教育部高等学校博士学科点专项科研基金新教师类（项目号：20090001120098）

  • Received:2012-07-15 Online:2012-10-12 Published:2013-01-04

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摘要： 【摘要】目的 通过对伴IgA沉积的微小病变肾病综合征(MCNS-IgA)患者血清中IgA1分子糖基化缺陷程度的检测，探讨MCNS-IgA的可能的病理分类归属。 方法  选择北京大学人民医院肾内科MCNS-IgA患者10人，微小病变肾病综合症(MCNS)患者10人、大量蛋白尿IgAN(H-IgAN)患者10人为对照。用双抗体夹心ELISA法检测各组患者血清IgA1的相对浓度，用黑木凝集素检测IgA1分子的a2，6唾液酸水平，花生凝集素检测IgA1分子的半乳糖水平，蜗牛凝集素检测IgA1分子的N-乙酰氨基半乳糖水平，计算经血清IgA1浓度校正的各糖基水平。观察MCNS-IgA组患者血清IgA1分子糖基化缺陷情况，并且与H-IgAN及MCNS组进行比较。 结果 与MCNS组相比，MCNS-IgA肾病患者血清IgA1的a2，6唾液酸(1.232±0.250比较1.379±0.623，P=0.455)、半乳糖缺失(0.204±0.053 vs 0.229±0.088，p=0.454)水平及N-乙酰氨基半乳糖暴露(0.191±0.039 vs 0.205±0.068, P=0.626)水平无明显差异。但其血清IgA1分子α2，6 唾液酸缺失(1.232±0.250 vs 0.756±0.243，P=0.015)及N-乙酰氨基半乳糖的暴露(0.191±0.039比较 0.258±0.066，P=0.025)显著低于H-IgAN组，半乳糖缺失少，但未达统计学差异(0.204±0.053比较 0.139±0.038，P=0.052)。 结论 MCNS-IgA组患者血清IgA1糖基化水平上显示了与IgA肾病不同的特点，提示其可能是微小病变伴IgA分子的非特异性沉积。

关键词: 伴IgA沉积的微小病变肾病综合征, 血清IgA1 a2, 6唾液酸, 半乳糖, N-乙酰氨基半乳糖

Abstract: 【Abstract】Objective To test the different degree of glycosylation of serum IgA1 among MCNS-IgA, H-IgAN, MCNS, in order to investigate the relationship between MCNS-IgA and IgAN. Methods Sera from 30 patients were collected. 10 of them were MCNS-IgA, 10 patients were H-IgA and the rest were MCNS used as controls. Biotinylated lectins were used in ELISA to examine different glycans on serum IgA1 molecules. The α 2,6 sialic acid was detected by elderberry bark lectin (SNA), the exposure of terminal galactose (Gal) and N-acetylgalactosamine (GalNAc) were detected by arachis hypogaea (PNA) and Helix asperas agglutinin (HAA), respectively. The IgA1 glycans levels, corrected by IgA1 concentrations, were compared between patients and controls.  Results Reduced terminal α 2,6 sialic acid (1.232±0.250 vs. 0.756±0.243, P=0.015), and increased exposure of N-acetylgalactosamine (0.191±0.039 vs. 0.258±0.066, P=0.025) were demonstrated in serum IgA1 from patients with H-IgAN as compared in that from MCNS-IgA. However, MNCS and MCNS-IgA had no significant differences among the levels of glycosylation (P＞0.05).  Conclusion MCNS-IgA shows the characteristics of IgA nephropathy in serum IgA1 glycosylation level, suggesting the presence of MCD with non-specific mesangial IgA molecule deposition.

Key words: Minimal change nephrotic syndrome with mesangial IgA deposition, Serum IgA, Sialic acid, Galactose, N-acetylgalactosamine