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Resolution of thrombotic microangiopathy following renal transplant.

Thrombotic microangiopathy (TMA) is characterized by aggregation of platelets in the renal and/or systemic circulation, thrombocytopenia and intravascular haemolysis. TMA is well recognized in the setting of renal transplantation and has been attributed to a variety of aetiologies such as recurrence of original disease, use of calcineurin inhibitors, acute rejection and viral infections [1,2]. Thrombotic thrombocytopenic purpura (TTP) and haemolytic uraemic syndrome (HUS) represent the two most frequently encountered clinical presentations of TMA. There is considerable overlap in the clinical features of HUS and TTP and it is often difficult to distinguish between these entities. Moreover, in the setting of renal transplantation, both entities have been described, suggesting that the same underlying mechanism may result in TTP in some individuals and HUS in others [1]. The commonality between these syndromes makes it tempting to lump them together into the single entity of TMA. There are, however, important differences in the underlying disease mechanisms that may have prognostic and therapeutic implications, particularly in the setting of renal transplantation [3].