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A spectrum of novel anti-vascular endothelial cells autoantibodies in idiopathic nephrotic syndrome patients

Idiopathic nephrotic syndrome (INS) is a common renal disease characterized by disruption of the glomerular filtration barrier. In a previous study, we screened and identified podocyte autoantibodies in nephrotic syndrome patients and proposed the concept of autoimmune podocytopathy. However, circul...

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Published in:Clinical immunology (Orlando, Fla.) Fla.), 2023-04, Vol.249, p.109273-109273, Article 109273
Main Authors: Ye, Qing, Wang, Dongjie, Zhou, Chao, Meng, Hanyan, Liu, Huihui, Mao, Jianhua
Format: Article
Language:English
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Summary:Idiopathic nephrotic syndrome (INS) is a common renal disease characterized by disruption of the glomerular filtration barrier. In a previous study, we screened and identified podocyte autoantibodies in nephrotic syndrome patients and proposed the concept of autoimmune podocytopathy. However, circulating podocyte autoantibodies cannot reach podocytes unless glomerular endothelial cells have been damaged. Therefore, we speculate that INS patients may also have autoantibodies against vascular endothelial cells. Sera from INS patients were used as primary antibodies to screen and identify endothelial autoantibodies by hybridization with vascular endothelial cell proteins separated by two-dimensional electrophoresis. The clinical application value and pathogenicity of these autoantibodies were further verified by clinical study and in vivo and in vitro experiments. Nine kinds of autoantibodies against vascular endothelial cells were screened in patients with INS, which can cause endothelial cell damage. In addition, 89% of these patients were positive for at least one autoantibody. The two-hit hypothesis of Autoimmune Podocytopathies: the pathogenic process of INS is first initiated by damage caused by pathogenic factors such as antiantibodies to glomerular endothelial cells, and subsequently, podocytes are exposed to those causative factors that lead to the occurrence of disease. [Display omitted]
ISSN:1521-6616
1521-7035
DOI:10.1016/j.clim.2023.109273