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伴有和不伴有肾小球足细胞消失的蛋白尿。

Proteinuria with and without renal glomerular podocyte effacement.

作者信息

Kalluri Raghu

机构信息

Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA.

出版信息

J Am Soc Nephrol. 2006 Sep;17(9):2383-9. doi: 10.1681/ASN.2006060628. Epub 2006 Aug 16.

DOI:10.1681/ASN.2006060628
PMID:16914535
Abstract

Renal biopsies of patients with proteinuria and kidney disease most often are associated with podocyte foot process effacement. For several decades, nephrologists have wondered whether proteinuria is a result of podocyte foot process effacement or the cause of it. In the past few years, the author's laboratory has addressed this issue using different mouse models of proteinuria. Although in most cases, podocyte effacement is associated with proteinuria and glomerular disease, in three different mouse models, it was demonstrated that proteinuria can be observed without podocyte foot process effacement. The first model is generated by injection of antibodies to vascular endothelial growth factor or soluble vascular endothelial growth factor receptor 1. The second model is a mouse with deletion of type IV collagen alpha3 chain in the glomerular basement membrane. The third model was generated by genetic deletion of a slit diaphragm protein known as nephrin. Collectively, these experiments and the supporting evidence from several human studies demonstrate that severe defects in either the glomerular basement membrane or the glomerular endothelium can lead to proteinuria without foot process effacement.

摘要

蛋白尿和肾病患者的肾活检大多与足细胞足突消失有关。几十年来,肾病学家一直想知道蛋白尿是足细胞足突消失的结果还是其原因。在过去几年里,作者所在实验室利用不同的蛋白尿小鼠模型解决了这个问题。虽然在大多数情况下,足细胞消失与蛋白尿和肾小球疾病相关,但在三种不同的小鼠模型中,已证明在没有足细胞足突消失的情况下也可观察到蛋白尿。第一个模型是通过注射抗血管内皮生长因子或可溶性血管内皮生长因子受体1的抗体构建的。第二个模型是肾小球基底膜中IV型胶原α3链缺失的小鼠。第三个模型是通过基因敲除一种名为nephrin的裂孔隔膜蛋白构建的。总的来说,这些实验以及来自几项人体研究的支持证据表明,肾小球基底膜或肾小球内皮的严重缺陷可导致无足突消失的蛋白尿。

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