Mannose-Binding Lectin Levels Could Predict Prognosis in IgA Nephropathy
Mannose-Binding Lectin Levels Could Predict Prognosis in IgA Nephropathy
复制标题
甘露糖结合凝集素水平可以预测 IgA 肾病的预后
DOI：
10.1681/asn.2017010076
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发表时间：
2017-11-01
影响因子：
13.6
通讯作者：
Zhang, Hong
中科院分区：
文献类型：
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作者：
Guo, Wei-yi;Zhu, Li;Zhang, Hong
伊加肾病（IgAN）的特征是感染后伴有发作性肉眼血尿。甘露糖结合凝集素（MBL）的缺乏与许多疾病的复发性感染有关，但关于MBL在IgAN中的作用存在争议。在这里，我们测量了749名IgAN患者和489名健康对照者的MBL 2变体和MBL水平。总体而言，5.2%（39/749）的IgAN患者存在MBL缺乏（MBL水平< 100 ng/ml），其中LYPB/LYPB和LXPA/LYPB是主要的MBL 2单倍型（82%; 32/39）。我们发现MBL水平与IgAN的肾脏预后呈非线性相关。IgAN和MBL缺乏的患者比MBL水平充足（100-3540 ng/ml）的患者有更高的前驱感染和肉眼血尿的发生率。此外，MBL缺乏与IgAN患者在多次校正后的肾脏预后不良独立相关（风险比，5.18; 95%可信区间，2.50 - 10.72; P < 0.001）。高MBL水平的患者（。3540 ng/ml）有更严重的蛋白尿和更高比例的新月体，尽管调整后与IgAN进展的相关性没有达到统计学显著性。总之，MBL缺乏和MBL过量都可能对IgAN的进展产生有害影响，这表明MBL通过多种机制参与IgAN的发病。
IgA nephropathy (IgAN) is characterized by infections followed by episodic gross hematuria. Deficiency of mannose-binding lectin (MBL) is associated with recurrent infection in many diseases, but controversy exists regarding the role of MBL in IgAN. Here, we measured MBL2 variants and MBL levels in 749 patients with IgAN and 489 healthy controls. Overall, 5.2% (39 of 749) of patients with IgAN had MBL deficiency (MBL levels < 100 ng/ml), among whom LYPB/LYPB and LXPA/LYPB were the predominant MBL2 haplotypes (82%; 32 of 39). We found a nonlinear association between MBL levels and renal outcome in IgAN. Patients with IgAN and MBL deficiency had a higher incidence of prodromic infections and gross hematuria than those with sufficient MBL levels (100-3540 ng/ml). Moreover, MBL deficiency independently associated with poor renal outcome in IgAN after multiple adjustments (hazard ratio, 5.18; 95% confidence interval, 2.50 to 10.72; P < 0.001). Patients with high MBL levels (. 3540 ng/ml) had more severe proteinuria and a higher proportion of crescents, although the association with IgAN progression did not reach statistical significance after adjustments. In conclusion, MBL deficiency and MBL excess may both have deleterious effects on IgAN progression, which suggests that MBL contributes to IgAN pathogenesis through multiple mechanisms.