Abstract
The pathogenesis of steroid- sensitive nephrotic syndrome (SSNS) is poorly defined. We previously demonstrated that monocytes from SSNS patients with proteinuria were activated to display exaggerated phagocytosis of opsonized particles and paradoxically reduced chemotaxis. In this study, we evaluated the capacity of hydrogen peroxide (H2O2) release from monocytes in 19 patients with SSNS and 13 healthy controls, by exposure to phorbol myristate acetate (PMA), using scopoletin method. Of 19 patients of SSNS, 7 were proteinuric and 12 in remission. The H2O2 release was significantly higher in SSNS patients with proteinuria than those in remission or normal controls [177.49±94.75 (mean±S.D.) vs. 60.67±58.89 (p<0.02) or 85.02± 48.62 nmol/90 min/mg cell protein (p<0.05)]. Follow-up measurements in two SSNS patients showed that H2O2 release was reduced when proteinuric condition was improved to be in remission. Our data suggest that monocytes in SSNS with proteinuria were activated and were prepared to receive some extracellular signaling leading to protein kinase-C activation for releasing H202.
