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链脲佐菌素诱导的糖尿病大鼠自体免疫复合物肾炎

Autologous immune complex nephritis in streptozotocin-induced diabetic rats.

作者信息

Okuda S, Oh Y, Onoyama K, Fujimi S, Omae T

出版信息

Nephron. 1984;37(3):166-73. doi: 10.1159/000183238.

DOI:10.1159/000183238
PMID:6234473
Abstract

In order to investigate the influence of diabetes mellitus on immune complex-mediated nephritis , we produced Heymann nephritis in streptozotocin-induced diabetic rats (DM-HN group) in which the clinical course for 24 weeks and histological changes were examined. Nondiabetic rats with Heymann nephritis (HN group) and diabetic rats (DM group) were also examined as controls. The degree of proteinuria, hypoproteinemia, hyperlipidemia and anemia were more pronounced and the mortality rate was higher in the DM-HN group than in the HN group or in the DM group. Histologically, larger and more subepithelial or intramembranous electron-dense deposits as well as a more markedly thickened glomerular basement membrane (GBM) were observed in the DM-HN group than in the HN group. In conclusion, the nephrotic manifestations and histological changes in the GBM in Heymann nephritis were augmented by the association with diabetes mellitus.

摘要

为了研究糖尿病对免疫复合物介导性肾炎的影响,我们在链脲佐菌素诱导的糖尿病大鼠(糖尿病-海曼肾炎组)中诱发了海曼肾炎,并对其24周的临床病程和组织学变化进行了检查。同时,将非糖尿病性海曼肾炎大鼠(海曼肾炎组)和糖尿病大鼠(糖尿病组)作为对照进行检查。糖尿病-海曼肾炎组的蛋白尿、低蛋白血症、高脂血症和贫血程度更为明显,死亡率也高于海曼肾炎组或糖尿病组。组织学检查发现,与海曼肾炎组相比,糖尿病-海曼肾炎组有更大、更多的上皮下或膜内电子致密沉积物,以及更明显增厚的肾小球基底膜(GBM)。总之,海曼肾炎的肾病表现和GBM的组织学变化因合并糖尿病而加重。

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Autologous immune complex nephritis in streptozotocin-induced diabetic rats.链脲佐菌素诱导的糖尿病大鼠自体免疫复合物肾炎
Nephron. 1984;37(3):166-73. doi: 10.1159/000183238.
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