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Objective: Minimal change disease (MCD) is the most common cause of nephrotic syndrome in childhood but its pathogenesis remains poorly understood. A T-cell-derived factor or factors were initially alleged as contributing to the disease pathogenesis. However, podocyte CD80 expression is now a commonly discussed theory. The aim of this study was to investigate the pathogenesis of MCD by determining urine interleukin-13, CD80, CD28, matrix metalloproteinase-2 (MMP-2), and granzyme B levels.\udMethods: Thirty patients and thirty healthy children were evaluated in this study. Six patients had biopsy proven MCD. The remaining patients were considered to have MCD because of their age at time of diagnosis; response to steroid treatment, absence of gross hematuria, hypocomplementemia or renal failure; and normal blood pressures in the active stage. The nephrotic-phase urine interleukin-13, CD80, CD28, MMP-2, and granzyme B levels of all patients were compared with the remission-stage urine levels of the same patients and control subjects. The urine samples were collected immediately before the application of immunosuppressive drugs or other treatment modalities.\udResults: Significantly higher interleukin-13, CD80, CD28, and MMP-2 levels were observed in the relapse period compared with both the remission period and control subjects. There was a significant positive correlation between the active-stage urine interleukin-13 and CD80 levels (r=0.619, p<0.001).\udConclusion: Interleukin-13, CD80, CD28, and MMP-2 seem to have roles in the pathogenesis of MCD and using inhibitors of these molecules in treatment of steroid and immunosuppressive-resistant MCD cases can be thought. J Clin Exp Invest 2014; 5 (3): 354-36

journal of clinical and experimental investigations

The roles of urine interleukin-13, CD80, CD28, matrix metalloproteinase-2 and granzyme B in the pathogenesis of childhood minimal change nephrotic syndrome