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Plasma Therapy (plasma + therapy)
Selected AbstractsExcellent response of refractory life-threatening thrombotic thrombocytopenic purpura to cyclosporine treatmentINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2004M. Itälä Summary The introduction of plasma exchange has significantly improved the outcome of thrombotic thrombocytopenic purpura (TTP), and survival has increased from 10 to 80,90%. TTP refractory to plasma exchange therapy, however, is still a therapeutic challenge. We describe here a patient who partially responded to plasma exchange therapy, but remained totally dependent on plasma infusions. Several attempts to discontinue plasma therapy repeatedly lead to relapses. TTP did not response to vincristine, either. After 3 months treatment with plasma therapy, cyclosporine was started. Plasma therapy could be discontinued after 3 weeks on cyclosporine, and serum LDH and blood platelet count were gradually normalized during 2 months. Cyclosporine was tapered off after 6 months treatment, and the patient has stayed in remission ever since. We conclude that cyclosporine is a worthwhile treatment option in patients with refractory TTP. [source] Thrombotic Microangiopathy After Kidney TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2010M. Noris Thrombotic microangiopathy (TMA) is a severe complication of kidney transplantation that often causes graft failure. TMA may occur de novo, often triggered by immunosuppressive drugs and acute antibody-mediated rejection, or recur in patients with previous history of hemolytic uremic syndrome (HUS). Recurrent TMA is very rare in patients who had developed end-stage renal failure following HUS caused by Shiga-toxin producing E. scherichia coli, whereas disease recurrence is common in patients with atypical HUS (aHUS). The underlying genetic defect greatly impacts the risk of posttransplant recurrence in aHUS. Indeed recurrence is almost the rule in patients with mutations in genes encoding factor H or factor I, whereas patients with a mutation in membrane-cofactor-protein gene have a good transplant outcome. Prophylactic and therapeutic options for posttransplant TMA, including plasma therapy, combined kidney and liver transplantation and targeted complement inhibitors are discussed in this review. [source] Successful Renal Transplantation in Factor H Autoantibody Associated HUS with CFHR1 and 3 Deficiency and CFH Variant G2850TAMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2010A. M. Waters Factor H (CFH) autoantibodies are associated with atypical hemolytic uremic syndrome (aHUS). Peritransplantation plasma exchange therapy and intensification of immunosuppression, with adjuvant use of anti-CD20 monoclonal antibodies has recently been advocated for cases of CFH-autoantibody associated aHUS. In this report, we describe successful deceased donor renal transplantation in a case of CFH-autoantibody associated aHUS with combined CFHR1 and 3 deficiency in addition to the CFH sequence variant, (cG2850T, pGln950His). CFH-autoantibodies were detected 2 weeks prior to transplantation. Disease recurrence was not observed using basiliximab, an IL2-receptor antagonist and high-dose corticosteroids with mycophenolate mofetil. Adjuvant therapies such as Rituximab nor intensification of plasma therapy were employed. Consequently, careful consideration needs to be given to the use of additional immunosuppression in certain cases of CFH-autoantibody associated aHUS. Serial measurement of CFH-autoantibodies is required in the immediate pre- and posttransplantation period to further clarify their role as a factor in the recurrence of aHUS posttransplantation. Furthermore, delineation of the functional significance of CFH-autoantibodies is warranted in individual cases. [source] | ||||||||||