Interferon gamma: is it a co-player in the pathogenesis of idiopathic nephrotic syndrome?

Abstract

Introduction: Idiopathic nephrotic syndrome (INS), the most common form of NS in childhood, was considered 4 decades ago as a systemic disorder of T cells, mediated through its released cytokines. To date, the exact incriminated cytokine or immunological mediator is not properly defined. Interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, is thought to have a role in the provocation of the T cell-mediated INS relapse, through the promotion of T helper1 (Th1) differentiation and suppression of regulatory T cells (Treg). Aim of the study: To evaluate the immunopathogenic role of IFN-gamma in children with steroid-sensitive idiopathic nephrotic syndrome (SSNS) through monitoring the changes in its levels with disease course. Methods: This study included twenty-five newly diagnosed children with SSINS. They were all given full dose prednisolone, evaluated at initial diagnosis and at full remission as regards the serum level of IFN-gamma. Results: Serum levels of IFN-gamma were lowermost at the time of diagnosis and increased with remission on corticosteroids. Conclusions: This study points to a role for the lower serum IFN-gamma at diagnosis, in the immunopathogenesis of INS than at remission and the rise in its serum level might be a marker of remission induction, however, this awaits confirmation in larger-scale studies. Studies on renal biopsy specimens are needed to determine the exact renal in situ levels and effects of IFN-gamma