S Kiyama, T Sakemi, T Shimokama, N Baba, T Watanabe
{"title":"Crescentic glomerulonephritis associated with renal amyloidosis.","authors":"S Kiyama, T Sakemi, T Shimokama, N Baba, T Watanabe","doi":"10.2169/internalmedicine1962.30.238","DOIUrl":null,"url":null,"abstract":"<p><p>A case of crescentic glomerulonephritis associated with renal amyloidosis is reported. A 62-year-old woman with a 6-yr history of rheumatoid arthritis developed rapidly progressive glomerulonephritis associated with renal amyloidosis and crescent formation. Amyloid protein was positively stained with anti-AA antibody and its fibrils were demonstrated by electron microscopy. In connection with epithelial cell proliferation in the capsular space, destruction of the capillary basement membrane was observed at the sites where amyloid fibrils were accumulated, whereas glomerular deposition of immunoglobulin and complement was not detected. It is conceivable that the destruction of the glomerular tufts induced by amyloid deposition may be responsible for the crescent formation.</p>","PeriodicalId":14798,"journal":{"name":"Japanese journal of medicine","volume":"30 3","pages":"238-42"},"PeriodicalIF":0.0000,"publicationDate":"1991-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2169/internalmedicine1962.30.238","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Japanese journal of medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2169/internalmedicine1962.30.238","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 8
Abstract
A case of crescentic glomerulonephritis associated with renal amyloidosis is reported. A 62-year-old woman with a 6-yr history of rheumatoid arthritis developed rapidly progressive glomerulonephritis associated with renal amyloidosis and crescent formation. Amyloid protein was positively stained with anti-AA antibody and its fibrils were demonstrated by electron microscopy. In connection with epithelial cell proliferation in the capsular space, destruction of the capillary basement membrane was observed at the sites where amyloid fibrils were accumulated, whereas glomerular deposition of immunoglobulin and complement was not detected. It is conceivable that the destruction of the glomerular tufts induced by amyloid deposition may be responsible for the crescent formation.