Thrombotic microangiopathy is rare but well recognized post transplant complication. The incidence of this syndrome varies among different transplant centers, primarily because of the lack of a uniform definition.
Patients and Methods: We retrospectively analyzed our data from medical records of 950 kidney recipients under follow up in our center since December 1994. We looked at the risk factors and basic criteria for diagnosis of the syndrome in these cases. We reviewed the kidney biopsies performed for these patients to exclude other conflicting diagnoses like antibody mediated rejection.
Results: HUS was diagnosed in 12 patients. 4 patients were male and 8 were females. None of them had HUS as the original kidney disease. Cyclosporine (CsA) was the primary immunosuppression in 10 and tacrolimus (Tac) in 2 patients. The median day of onset of HUS post transplant was 7 days. Criteria for diagnosis were anaemia (100%), thrombocytopenia (75%), elevated reticulocyte count (62.5%), fragmented red cells in blood smear (8.3%), elevated lactate dehydrogenase [LDH] enzyme (83.3%), increased fibrin degradation product [FDP] (83.3%), reduced haptoglobin level (42.9%) and hyperbilirubinemia (25%). Calcineurin inhibitor (CNI) elimination was the first step in the management. Transfusion of fresh frozen plasma [FFP] was used in 10 patients and plasma exchange [PE] using FFP as a replacement agent in the other two. All grafts recovered function. Two patients had reintroduction of CsA or Tac after complete clinical and laboratory recovery of CNI induced HUS. Both developed recurrence of HUS. While the former did not the later did recover on further treatment of HUS. Early CNI discontinuation and plasma replacement therapy can revert CNI induced HUS and save the graft. Reintroduction of CNI is deleterious to the graft and should be avoided.