期刊
PEDIATRIC RESEARCH
卷 64, 期 6, 页码 637-642出版社
NATURE PUBLISHING GROUP
DOI: 10.1203/PDR.0b013e318186ddb2
关键词
-
类别
资金
- FAPEMIG (Fundacao de Amparo a Pesquisa do Estado de Minas Gerais, Brazil)
- CNPq (Conselho Nacional de Desenvolvimento Cientifico a Tecnologico, Brazil)
- PRONEX (Programa de Grupos do Excelencia-FINEP, Brazil)
The pathogenesis of idiopathic nephrotic syndrome (INS) remains unknown. Several findings suggest a role for the immune system. This study aimed to evaluate immune mediators in INS by measuring plasma and urinary levels of transforming growth factor beta(1) (TGF-beta(1)), monocyte chemoattractant protein-1 (MCP-1/ CCL2), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and IL-8 (IL-8/CXCL8) in pediatric patients with INS and in age-matched healthy controls. Patients were divided according to their response to corticosteroids: steroid-sensitive (SS, n = 8), or steroid-resistant (SR, n = 24). Immune mediators were also compared in regard with disease activity (relapse and remission). Immune mediators were measured by ELISA. Plasma TGF-beta(1) levels in SR patients were approximately 2.8-fold higher than control values (p < 0.05). Urinary IL-8/CXCL8 was 2.9-fold higher in INS patients in relapse (proteinuria >100 mg/m(2)-/24 h) when compared with patients in remission (p < 0.05), and levels had a positive correlation with individual proteinuria values (p < 0.05). Urinary IL-8/CXCL8 was significantly higher in relapsed SR than in SS patients in remission. No changes in MCP-1/CCL2 and RANTES/CCL5 levels were detected. Our findings suggest that IL-8/CXCL8 and TGF-beta(1), are involved in the pathogenesis of INS: IL-8/CXCL8 associated with local changes in glomerular permeability and TGF-beta(1), could be related to worse response to corticosteroids. (Pediatr Res 64: 637-642,2008)
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据