A 5-year-old girl received a cadaver kidney transplant 2 years after a
typical hemolytic uremic syndrome (HUS) leading to end-stage renal fai
lure. Azathioprine (AZA) (1.5 mg/kg per day), prednisone (2 mg/kg per
day), and rabbit antithymocyte globulin (ATG) (4 mg/kg on alternate da
ys) were used as rejection prophylaxis. Impaired renal function never
allowed discontinuation of continuous ambulatory peritoneal dialysis.
After the second ATG administration (day 3), progressive anemia [hemog
lobin (Hb) 5.5 mmol/l] thrombopenia (19x109/l) without leukopenia (4.2
x109/l), and a small increase in lactic dehydrogenase (LDH) (350 U/l)
were observed (day 6). Because of persistent thrombopenia, AZA and ATG
were stopped on day 3 and cyclosporin A (CsA) was started on day 6. O
n day 7, anemia was more profound (Hb 4 mmol/l), and hemolysis obvious
(LDH 2,150 U/l, numerous fragmentocytes, negative Coombs' test). CsA
was immediately stopped and replaced by mycophenolate, without improve
ment of renal function. Kidney biopsy showed an arteriolar microangiop
athy without rejection. Transplantectomy was performed (day 18). Was A
TG the cause of HUS recurrence? What approach do you advise now?.