Kawaguchi K, Koike M
Department of Pathology, Tokyo Metropolitan Komagome Hospital, Japan.
Hum Pathol. 1987 Nov;18(11):1149-54. doi: 10.1016/s0046-8177(87)80383-0.
An immunohistochemical and clinicopathologic analysis of glomerular alterations was carried out in 20 autopsy cases with obstructive jaundice. The 20 cases without clinical nephritis had primary carcinoma of various locations, including the stomach, rectum, pancreas, and biliary tract. Mesangial IgA deposition was present on immunofluorescence staining in four cases, IgG in two cases, IgM in five cases, and C3 in four cases. Glomerular polymeric IgA containing A1, A2, and J chain was considered to originate from the gastrointestinal tract. All immunofluorescence-positive cases except one had electron-dense deposits in mesangial regions. These findings suggest that glomerular IgA deposition develops in a handful of patients suffering from obstructive jaundice, presumably due to the passive trapping of circulating immune complexes. Furthermore, glomerular IgA deposition in patients with obstructive jaundice is not influenced by duration or intensity of jaundice, and it unlikely induces clinical nephritis.
对20例梗阻性黄疸尸检病例进行了肾小球改变的免疫组织化学和临床病理分析。这20例无临床肾炎的病例患有各种部位的原发性癌,包括胃、直肠、胰腺和胆道。免疫荧光染色显示,4例有系膜IgA沉积,2例有IgG沉积,5例有IgM沉积,4例有C3沉积。含有A1、A2和J链的肾小球聚合IgA被认为起源于胃肠道。除1例外,所有免疫荧光阳性病例在系膜区均有电子致密沉积物。这些发现表明,少数梗阻性黄疸患者会发生肾小球IgA沉积,可能是由于循环免疫复合物的被动捕获所致。此外,梗阻性黄疸患者的肾小球IgA沉积不受黄疸持续时间或强度的影响,也不太可能诱发临床肾炎。