Pathogenesis of IgA nephropathy.
Pathogenesis of IgA nephropathy.
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DOI：
10.1159/000102280
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发表时间：
2007
影响因子：
--
通讯作者：
Y. Tomino
中科院分区：
文献类型：
--
作者：
Y. Tomino
IgA肾病通常被认为是免疫复合物介导或聚集（聚合）IgA （IgA1）介导的肾小球肾炎。由于IgA肾病的发病机制尚不清楚，因此利用自发动物模型来确定这种疾病的发生和进展是很重要的。ddY小鼠品系可作为IgA肾病的自发性动物模型。遗传因素被认为参与了IgA肾病的发生和发展。据推测，IgA肾病的易感基因可以通过使用该模型的全基因组扫描来检测。10号染色体上的峰值标记D10MIT 86位于与人类6q22-23与IGAN1同源的区域，这是常见的IgA肾病的原因。这种疾病有几个发展和/或加重因素。其中肾小球上皮细胞（足细胞）的丢失和间质肥大细胞的浸润是IgA肾病患者肾小球硬化和小管间质损伤进展的重要因素。
IgA nephropathy is generally considered to be an immune-complex-mediated or aggregated (polymerized) IgA (IgA1)-mediated glomerulonephritis. Since the pathogenesis of IgA nephropathy is still obscure, it is important to determine the initiation and progression of this disease using the spontaneous animal model. The ddY mouse strain can serve as a spontaneous animal model for IgA nephropathy. Genetic factors are considered to be involved in the initiation and progression of IgA nephropathy. It has been hypothesized that susceptibility genes for IgA nephropathy can be detected by a genome-wide scan using this model. The peak marker D10MIT 86 on chromosome 10 is located on the region syntenic to human 6q22-23 with IGAN1, which is responsible for familiar IgA nephropathy. There are several developmental and/or exacerbating factors in this disease. Among them, the loss of glomerular epithelial cells (podocytes) and interstitial mast cell infiltration are important factors for progression of glomerulosclerosis and tubulointerstitial injury in patients with IgA nephropathy.