Cyclosporine A (CsA) has been accepted as one of the most efficient therapies of idiopathic nephrotic syndrome (INS) in children. Despite its beneficial effect on clinical course of the disease, its use has been associated with a number of side-effects. This prompted us to study the influence of cyclosporine A on the coagulation cascade in nephrotic children. We examined thrombinogenesis in 16 children in remission of steroid-dependent idiopathic nephrotic syndrome treated with cyclosporine A. The concentrations of F1 + 2 prothrombin fragments and thrombin-antithrombin complexes were used as markers of coagulation cascade activation. The results were compared between 18 children with INS relapse who had responded to 8-week glucocorticoid treatment (not treated with cyclosporine A) and 20 healthy subjects. We found an increased concentration of F1 + 2 prothrombin fragments in children treated with CsA, while in children after 8 weeks of glicocorticoid therapy the concentration of this marker was comparable to that in the controls. Since we observed similar biochemical disturbances in both INS groups, we suggested that cyclosporine A was able to stimulate coagulation that might lead to an increased risk of thomboembolic events in children with clinical remission of INS.