Thrombotic microangiopathy is an uncommon but well described complicat
ion of renal transplantation. This study is a review of the case recor
ds of Is patients with biopsy proven post transplant thrombotic microa
ngiopathy, without cellular rejection. There was no single characteris
tic underlying cause of renal failure in native kidneys. Although only
two (11%) patients had undergone previous transplantation, 16 (89%) h
ad panel reactive antibodies (PRA). All patients received prophylactic
antilymphocyte globulin, a single patient had cyclosporin A (CSA) at
the time of transplant and in 16 patients CSA was introduced when graf
t function was established. On this protocol 16 (89%) patients had ear
ly graft function. All patients developed acute renal failure and 16 (
89%) required dialysis. Nine (50%) patients developed hematological ab
normalities. All patients were treated aggressively with anti-rejectio
n therapy, CSA was temporarily withdrawn, and 2 (11%) patients receive
d plasmapheresis. Seven (39%) patients lost their grafts. Renal functi
on in the remaining patients recovered to serum creatinine levels rang
ing from 104 mu mol/l to 430 mu mol/l (1.2 mg% to 4.8 mg%). All patien
ts with surviving grafts had CSA successfully reintroduced. This study
indicates that there is an association between patients who develop p
osttransplant thrombotic microangiopathy after CSA administration and
high PRA levels. The condition appears to respond to anti-rejection th
erapy and stopping CSA in the majority of cases. The safe reintroducti
on of CSA suggests that endothelial cell damage in the posttransplant
period may be multifactorial and not solely due to CSA therapy.