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A 5-year-old girl received a cadaver kidney transplant 2 years after atypical hemolytic uremic syndrome (HUS) leading to end-stage renal failure. Azathioprine (AZA) (1.5 mg/kg per day), prednisone (2 mg/kg per day), and rabbit antithymocyte globulin (ATG) (4mg/kg on alternate days) 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 [hemoglobin (Hb) 5.5 mmol/l], thrombopenia (19×10⁹/l) without leukopenia (4.2×10⁹/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. On 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 improvement of renal function. Kidney biopsy showed an arteriolar microangiopathy without rejection. Transplantectomy was performed (day 18). Was ATG the cause of HUS recurrence? What approach do you advise now?