Evaluation and management of steroid-sensitive nephrotic syndrome

This review examines new literature published in 2006 and 2007 on steroid-sensitive nephrotic syndrome.

Steroid-sensitive nephrotic syndrome has long been thought to be due to lymphocyte-derived circulating factors leading to podocyte injury with subsequent proteinuria. New studies support this mechanism and implicate the T helper 2 cytokine IL-13. In addition a genetic mutation in familial nephrotic syndrome has been reported in a child, who responded to corticosteroid therapy. There are new clinical trial data supporting the efficacy of levamisole in steroid-sensitive nephrotic syndrome and preliminary trial data on mycophenolate mofetil supporting its efficacy as a steroid-sparing agent. Case reports support the use of the B cell-depleting antibody rituximab in steroid-sensitive nephrotic syndrome. Finally there is a meta-analysis of six studies suggesting an increase in the incidence of focal and segmental glomerulosclerosis in steroid-sensitive nephrotic syndrome over the last 20 years.

Progress has been made towards elucidating the cause of steroid-sensitive nephrotic syndrome. Data from adequately powered randomized controlled trials are still required to evaluate therapies for frequently relapsing and steroid-dependent steroid-sensitive nephrotic syndrome.