Increase of tumour necrosis factor α synthesis and gene expression in peripheral blood mononuclear cells of children with idiopathic nephrotic syndrome

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Abstract
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 α (TNFα), a cytokine mainly produced by monocytes, in 25 children with idiopathic nephrotic syndrome. TNFα was determined by cytotoxicity bioassay in the L‐929 cell line and by double antibody/RIA. Patients in activity had higher serum TNFα levels and TNFα production by monocytes than patients in remission and controls. TNFα mRNA expression in blood mononuclear cells was analysed by Northern blot. The TNFα mRNA levels in patients in activity were increased compared to controls and to patients in remission. No significant differences in IL‐1β and IL‐6 synthesis were found between patients and controls. Our results suggest that TNFα, but not other cytokines such as IL‐1β and IL‐6, could play a role in the pathogenesis of the proteinuria in idiopathic nephrotic syndrome.