Interleukin-8 and tumor necrosis factor-alpha are increased in minimal change disease but do not alter albumin permeability

被引:24
作者
Cho, MH
Lee, HS
Choe, BH
Kwon, SH
Chung, KY
Koo, JH
Ko, CW
机构
[1] Kyungpook Natl Univ Hosp, Dept Pediat, Taegu 700721, South Korea
[2] Inst Biomed Res, Taegu, South Korea
关键词
minimal change nephrotic syndrome; interleukin-8; tumor necrosis factor-alpha; glomerular epithelial cell; albumin permeability;
D O I
10.1159/000072065
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Aims: Minimal change disease (MCD) is the most common primary nephrotic syndrome in children. Some suggested that interleukin-8 (IL-8) and tumor necrosis factora (TNF-alpha) are involved in the pathogenesis of MCD. This study was done to see changes of plasma and urinary IL-8, TNF-alpha, and their effects on determination of permeability of glomerular basement membrane (BM) contributed by heparan sulfate proteoglycan (HSPG). Methods: Study patients consisted of 19 biopsy-proven MCD children aged 2-15 years old. Both plasma, urinary IL-8 and TNF-alpha were measured. Employing the Millicell system, IL-8 and TNF-alpha were screened for the permeability factors. We examined whether IL-8 and TNF-alpha regulated BM HSPG gene expression and HS synthesis in the glomerular epithelial cells (GECs). Results: Urinary IL-8 during relapse was significantly increased when compared with that of during remission or controls (13,996 2,811 vs. 2,941 +/- 373, 5,331 +/- 640 ng/mg.cr) (p < 0.05). Urinary TNF-alpha during relapse was also significantly increased (364.4 +/- 51.2 vs. 155.3 +/- 20.8, 36.0 +/- 4.5 ng/mg . cr) (p < 0.05). Plasma IL-8 during relapse was significantly increased compared to that during remission (1.19 +/- 0.62 vs. 0.51 +/- 0.42 ng/ml) (p < 0.05). However, the negative results were obtained in the permeability assay using the Millicell system. No difference was seen in BM HSPG gene expression and HS synthesis in the GECs. Conclusion: Therefore, it seems that both IL-8 and TNF-alpha may not play a disease-specific role in the pathogenesis of MCD. Copyright (C) 2003 S. Karger AG, Basel.
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页码:260 / 266
页数:7
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