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青霉胺诱发肾小球疾病的免疫病理学

Immunopathology of penicillamine-induced glomerular disease.

作者信息

Dische F E, Swinson D R, Hamilton E B, Parsons V

出版信息

J Rheumatol. 1976 Jun;3(2):145-54.

PMID:950631
Abstract

Four patients with rheumatoid arthritis developed heavy proteinuria after five to 12 months of treatment with D-penicillamine. Light microscopy of renal biopsy samples showed minimal glomerular capillary wall thickening and mesangial matrix increase, or no departure from normal. Electron microscopy, however, revealed subepithelial electron-dense deposits, fusion of epithelial cell foot processes, and evidence of mesangial cell hyperactivity. Immunofluorescence microscopy demonstrated granular capillary wall deposits of IgG and C3. The findings were similar to those in early membranous glomerulonephritis, differences being observed however in the results of staining for the early-acting complement components C1q and C4. It is tentatively concluded that complement was activated by the classical pathway.

摘要

4例类风湿关节炎患者在接受青霉胺治疗5至12个月后出现大量蛋白尿。肾活检样本的光镜检查显示肾小球毛细血管壁轻度增厚和系膜基质增加,或无异常。然而,电镜检查发现上皮下电子致密沉积物、上皮细胞足突融合以及系膜细胞活性增强的证据。免疫荧光显微镜检查显示IgG和C3在毛细血管壁呈颗粒状沉积。这些发现与早期膜性肾小球肾炎相似,但在早期起作用的补体成分C1q和C4的染色结果上存在差异。初步得出结论,补体是通过经典途径激活的。

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