BACKGROUND: Hemolytic uremic syndrome (HUS)/thrombotic microangiopathy (TMA) (tissue-limited HUS) is a well-recognized serious complication of renal transplantation, affecting 3% to 14% patients who are administered calcineurin inhibitor-based immunosuppression. We performed a retrospective study to examine the incidence, etiology, course, and outcome of HUS/TMA in our experience. PATIENTS AND METHODS: This retrospective study of 1540 renal allograft biopsies performed between January 2000 and October 2007 was performed to assess the incidence of HUS/TMA. Institute Transplant Registry records were reviewed for clinical history, laboratory findings, medications, and outcome. The offending drug was substituted in all subjects and plasmapheresis was added as an adjuvant until recovery of allograft function. RESULTS: TMA was observed in 17 (1.1%) biopsies. Two of 17 patients experienced recurrent HUS; 15 were drug-induced (12 with cyclosporine, three with Sirolimus); 10 were TMA; and five HUS. Nine patients developed HUS/TMA within 3 months of transplantation with eight developing it within 1 year posttransplantation. Graft function recovered in 12, while five did not recover. The HUS group showed 60% recovery compared with 80% among the TMA group. Two patients were lost; both displayed HCV seropositivity and one also showed anti-cardiolipin antibody. CONCLUSION: Early allograft biopsy with prompt diagnosis and management by drug substitution +/- plasmapheresis in posttransplant HUS/TMA plays an important role in allograft outcome. TMA showed better recovery than HUS.
BACKGROUND:Hemolytic uremic syndrome (HUS)/thrombotic microangiopathy (TMA) (tissue-limited HUS) is a well-recognized serious complication of renal transplantation, affecting 3% to 14% patients who are administered calcineurin inhibitor-based immunosuppression. We performed a retrospective study to examine the incidence, etiology, course, and outcome of HUS/TMA in our experience. PATIENTS AND METHODS: This retrospective study of 1540 renal allograft biopsies performed between January 2000 and October 2007 was performed to assess the incidence of HUS/TMA. Institute Transplant Registry records were reviewed for clinical history, laboratory findings, medications, and outcome. The offending drug was substituted in all subjects and plasmapheresis was added as an adjuvant until recovery of allograft function. RESULTS:TMA was observed in 17 (1.1%) biopsies. Two of 17 patients experienced recurrent HUS; 15 were drug-induced (12 with cyclosporine, three with Sirolimus); 10 were TMA; and five HUS. Nine patients developed HUS/TMA within 3 months of transplantation with eight developing it within 1 year posttransplantation. Graft function recovered in 12, while five did not recover. The HUS group showed 60% recovery compared with 80% among the TMA group. Two patients were lost; both displayed HCV seropositivity and one also showed anti-cardiolipin antibody. CONCLUSION: Early allograft biopsy with prompt diagnosis and management by drug substitution +/- plasmapheresis in posttransplant HUS/TMA plays an important role in allograft outcome. TMA showed better recovery than HUS.