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  • 标题:Idiopathic nephrotic syndrome and the immune system
  • 本地全文:下载
  • 作者:Ihab Z. El-Hakim
  • 期刊名称:Egyptian Journal of Pediatric Allergy and Immunology
  • 印刷版ISSN:1687-1642
  • 电子版ISSN:2314-8934
  • 出版年度:2006
  • 卷号:4
  • 期号:1
  • 页码:30-32
  • 出版社:Egyptian Society of Pediatric Allergy and Immunology
  • 摘要:Childhood nephrotic syndromes are most commonly caused by one of two idiopathic diseases: minimal-change nephrotic syndrome (MCNS) and focal segmental glomerulosclerosis (FSGS). The cause of idiopathic nephrotic syndrome (INS) remains unknown, but evidence suggests that it may be a primary T-cell disorder that leads to glomerular podocyte dysfunction1.In 1974, Shalhoub postulated that INS might be secondary to a disorder of T-lymphocyte function2. He hypothesized that clonal expansion of a T-lymphocyte subpopulation might result in the production of lymphokines, which increase the permeability of the glomerular filtration barrier to proteins. Data supporting this hypothesis were the response of the disease to corticosteroids and alkylating agents; the remission occurring in association with measles, which depresses cell-mediated immunity; the susceptibility of patients to pneumococcal infections; and the occurrence of MCNS in patients with Hodgkin’s disease3.A 3-4-fold increased incidence of HLA-DR7 in children with INS has been reported4,5. An association with HLA-B8 was reported in Europe. Children with atopy and HLA-B12 have a 13-fold increased risk of developing INS3.
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