Cyclosporin A does not affect platelets in children with idiopathic nephrotic syndrome.

The immunosuppressive agents administered to maintain the remission of idiopathic nephrotic syndrome (INS) may have a deleterious effect on several cell types. The aim of this study was to analyze platelet activation and reactivity in children with INS treated with cyclosporin A (CyA). The study groups comprised 16 children with remission of INS induced by CyA and 16 children with glucocorticosteroid-induced remission 8 weeks from the onset of INS relapse. Fifteen healthy children served as controls. Surface expression of CD61, CD62P, and CD42b on resting and thrombin-stimulated platelets was analyzed with flow cytometry. No differences between groups were found in CD61, CD62P, and CD42b surface expression, but markers of the coagulation cascade and fibrinolysis or endothelial injury (F1+2 prothrombin fragments, tissue plasminogen activator inhibitor 1) were elevated in patients treated with CyA compared with children on steroids and healthy controls. No correlations between markers of platelet function and CyA concentration were found. We postulate that CyA administration in nephrotic patients causes an activation of thrombinogenesis but does not influence platelet activation and reactivity in INS.