Cyclosporine and tacrolimus-associated thrombotic microangiopathy

The development of thrombotic microangiopathy (TMA) associated with the use of cyclosporine has been well documented. Treatments have included discont inuation or reduction of cyclosporine dose with or without concurrent plasm a exchange, plasma infusion, anticoagulation, and intravenous immunoglobuli n G infusion, However, for recipients of organ transplantation, removing th e inciting agent is not without the attendant risk of precipitating acute r ejection and graft loss. The last decade has seen the emergence of tacrolim us as a potent immunosuppressive agent with mechanisms of action virtually identical to those of cyclosporine. As a result, switching to tacrolimus ha s been reported to be a viable therapeutic option in the setting of cyclosp orine-induced TMA, With the more widespread application of tacrolimus in or gan transplantation, tacrolimus-associated TMA has also been recognized. Ho wever, literature regarding the incidence of the recurrence of TMA in patie nts exposed sequentially to cyclosporine and tacrolimus is limited. We repo rt a case of a living donor renal transplant recipient who developed cyclos porine-induced TMA that responded to the withdrawal of cyclosporine in conj unction with plasmapheresis and fresh frozen plasma replacement therapy, In troduction of tacrolimus as an alternative immunosuppressive agent resulted in the recurrence of TMA and the subsequent loss of the renal allograft. P atients who are switched from cyclosporine to tacrolimus or vice versa shou ld be closely monitored for the signs end symptoms of recurrent TMA. (C) 20 00 by the National Kidney Foundation, Inc.