Transplant-associated thrombotic microangiopathy: the role of IgG administration as initial therapy.

Two transplant patients, one a renal-pancreas and the other a liver allograft recipient, are reported. Both developed clinical and histologic evidence of cyclosporine-associated thrombotic microangiopathy and responded favorably to intravenous IgG therapy. An additional 20 cadaveric renal transplant recipients who developed cyclosporine-associated thrombotic microangiopathy are reviewed. The clinical and laboratory presentation of posttransplant thrombotic microangiopathy varied. Elevated serum creatinine and lactic dehydrogenase (LDH) levels were the most consistent, albeit nonspecific, findings at diagnosis. Fourteen of 22 patients (64%) presented with thrombocytopenia and 19 (86%) had a hemolytic anemia verified on diagnosis. Histologic evidence of thrombotic microangiopathy was present in renal biopsies from each of the renal allograft recipients and a skin biopsy from the liver allograft recipient. Treatment included withdrawal or reduction of the cyclosporine dose, plasmapheresis, or administration of intravenous IgG. There was an overall renal allograft loss of 57%, which included five deaths. Symptomatic cytomegalovirus infection was more common than expected in this patient group (P = 0.038) and may, in combination with cyclosporine therapy, have predisposed these patients to develop clinically significant thrombotic microangiopathy. Transplant-associated microangiopathy appears to be a relatively common disorder associated with a substantial increase in early graft loss (P = 0.005) and mortality (P = 0.001).