Hirose H, Takemura Y, Honma S, Asano K, Fukui T, Satoh T, Sugiura H
Department of Internal Medicine, Kasumigaura National Hospital, Tsuchiura, Japan.
Jpn J Med. 1991 Mar-Apr;30(2):130-4. doi: 10.2169/internalmedicine1962.30.130.
A 67-year-old woman was admitted for nephrotic syndrome. In spite of the lack of lymphadenopathy, hepatosplenomegaly and serum hyperviscosity, remarkable monoclonal IgM-proteinemia was demonstrated. Amyloid kidney was shown by renal biopsy. However, in the bone marrow and other organs, neither proliferation nor invasion of monoclonal immunoglobulin-producing cells was revealed by immunohistological investigations of the specimens biopsied or examined at autopsy, excluding Waldenström's macroglobulinemia. Immunosuppressive chemotherapy with cyclophosphamide, vincristine and prednisolone was effective in reducing serum IgM, but could not slow the progression of renal failure. This case suggested the association of generalized amyloidosis with excessive IgM-proteinemia caused by a non-malignant mechanism.
一名67岁女性因肾病综合征入院。尽管没有淋巴结肿大、肝脾肿大和血清高粘滞血症,但仍显示出明显的单克隆IgM蛋白血症。肾活检显示为淀粉样肾病。然而,通过对活检标本或尸检标本进行免疫组织学检查,在骨髓和其他器官中均未发现单克隆免疫球蛋白产生细胞的增殖或浸润,排除了华氏巨球蛋白血症。环磷酰胺、长春新碱和泼尼松龙的免疫抑制化疗在降低血清IgM方面有效,但未能减缓肾衰竭的进展。该病例提示全身性淀粉样变性与非恶性机制导致的IgM蛋白血症过多有关。