THROMBOTIC MICROANGIOPATHY IN RENAL-TRANSPLANT RECIPIENTS TREATED WITH CYCLOSPORINE-A

Citation
R. Zent et al., THROMBOTIC MICROANGIOPATHY IN RENAL-TRANSPLANT RECIPIENTS TREATED WITH CYCLOSPORINE-A, Clinical nephrology, 47(3), 1997, pp. 181-186
Citations number
28
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
03010430
Volume
47
Issue
3
Year of publication
1997
Pages
181 - 186
Database
ISI
SICI code
0301-0430(1997)47:3<181:TMIRRT>2.0.ZU;2-X
Abstract
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 All patients were treated aggressively with anti-rejectio n therapy, CSA was temporarily withdrawn, and 2 (11%) patients receive d plasmapheresis.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.