Bustos C, González E, Muley R, Alonso J L, Egido J
Division of Nephrology, Fundación Jiménez Díaz, Universidad Autonoma, Madrid, Spain.
Eur J Clin Invest. 1994 Dec;24(12):799-805. doi: 10.1111/j.1365-2362.1994.tb02022.x.
The pathogenesis of idiopathic nephrotic syndrome (minimal change nephropathy and its variants) is not completely understood. In recent years it has been speculated that a cytokine released by circulating blood mononuclear cells could alter the permeability of the glomerular capillary wall. In this study we have explored the potential participation of tumour necrosis factor alpha (TNF alpha), a cytokine mainly produced by monocytes, in 25 children with idiopathic nephrotic syndrome. TNF alpha was determined by cytotoxicity bioassay in the L-929 cell line and by double antibody/RIA. Patients in activity had higher serum TNF alpha levels and TNF alpha production by monocytes than patients in remission and controls. TNF alpha mRNA expression in blood mononuclear cells was analysed by Northern blot. The TNF alpha mRNA levels in patients in activity were increased compared to controls and to patients in remission. No significant differences in IL-1 beta and IL-6 synthesis were found between patients and controls. Our results suggest that TNF alpha, but not other cytokines such as IL-1 beta and IL-6, could play a role in the pathogenesis of the proteinuria in idiopathic nephrotic syndrome.
特发性肾病综合征（微小病变肾病及其变异型）的发病机制尚未完全明确。近年来，有人推测循环血单核细胞释放的一种细胞因子可能会改变肾小球毛细血管壁的通透性。在本研究中，我们探讨了主要由单核细胞产生的细胞因子肿瘤坏死因子α（TNFα）在25例特发性肾病综合征患儿中的潜在作用。通过L-929细胞系的细胞毒性生物测定法和双抗体/放射免疫分析法测定TNFα。活动期患者的血清TNFα水平及单核细胞产生的TNFα高于缓解期患者和对照组。采用Northern印迹法分析血单核细胞中TNFα mRNA的表达。活动期患者的TNFα mRNA水平高于对照组和缓解期患者。患者与对照组之间IL-1β和IL-6合成无显著差异。我们的结果表明，TNFα而非其他细胞因子如IL-1β和IL-6可能在特发性肾病综合征蛋白尿的发病机制中起作用。
