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Atypical haemolytic–uraemic syndrome at the onset of acute promyelocytic leukaemia

A 68-year-old woman was admitted with fever and pancytopenia (white blood cell count 0AE9 · 10/l, haemoglobin 8 g/dl, platelet count 9 · 10/l). Bone marrow examination showed acute promyelocytic leukaemia; cytogenetic and molecular analysis showed t(15;17) and a PML-RARa fusion protein (BCR3 transcript). Laboratory findings at diagnosis were: blood urea nitrogen 12 mmol/l, creatinine 160 lmol/l, uric acid 0AE4 mmol/l, lactate dehydrogenase 2259 U/l, total bilirubin 42 lmol/l, unconjugated bilirubin 28 lmol/l and haptoglobin <0AE1 lmol/l. Direct and indirect Coombs’ tests were negative; fibrinogen, prothrombin time and activated partial thromboplastin time were normal with a D-dimer of 8AE5 lg/l. The peripheral blood film showed some schistocytes. Urinalysis showed microscopic haematuria and proteinuria. The patient was started on induction chemotherapy with all-trans retinoic acid 60 mg/d followed by idarubicin 10 mg/ m (four doses) according to the Gruppo Italiano Malattie Ematologiche dell’Adulto (GIMEMA) protocol. Despite chemotherapy and appropriate supportive therapy, including hydration and red cell transfusions, the acute renal failure worsened, with an increase in creatinine (150 lmol/l) and progressive oliguria for which haemodialysis was started (three times a week). Kidney ultrasound examination was normal. A renal biopsy showed thrombotic microangiopathy with predominant glomerular involvement (arteriolar congestion with thrombi and endothelial damage) without cortical atrophy or necrosis (figures). Direct immunofluorescent microscopy showed diffuse IgM deposition in the mesangium, glomerular capillary subendothelium and focal deposition along capillary walls of IgA and C4 with a marked subendothelial widening with double contours. The clinical and histological findings were in accordance with an atypical (without diarrhoeal prodrome) haemolytic-uraemic syndrome. Despite treatment with dialysis, dexamethasone, plasma infusion and plasma exchange, the acute renal failure did not improve and the patient died 5 weeks after the diagnosis of leukaemia in a condition of haematologic remission. Atypical haemolyticuraemic syndrome, although rare, can be a fatal complication at onset or during induction chemotherapy of acute myeloid leukaemia.