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We report two cases of non-cardiogenic pulmonary edema as a complication of basiliximab induction therapy in young pediatric renal transplant patients identified following a retrospective review of all pediatric renal transplant cases performed in the National Paediatric Transplant Centre, Childrens University Hospital, Temple Street, Dublin, Ireland. Twenty-eight renal transplantations, of which five were living-related (LRD) and 23 were from deceased donors (DD), were performed in 28 children between 2003 and 2006. In six cases, transplantations were pre-emptive. Immunosuppression was induced pre-operatively using a combination of basiliximab, tacrolimus and methylprednisolone in all patients. Basiliximab induction was initiated 2 h prior to surgery in all cases and, in 26 patients, basiliximab was re-administered on post-operative day 4. Two patients, one LRD and one DD, aged 6 and 11 years, respectively, developed acute non-cardiogenic pulmonary edema within 36 h of surgery. Renal dysplasia was identified as the primary etiological factor for renal failure in both cases. Both children required assisted ventilation for between 4 and 6 days. While both grafts had primary function, the DD transplant patient subsequently developed acute tubular necrosis and was eventually lost within 3 weeks due to thrombotic microangiopathy and severe acute antibody-mediated rejection despite adequate immunosuppression. Non-cardiogenic pulmonary edema is a potentially devastating post-operative complication of basiliximab induction therapy in young pediatric patients following renal transplantation. Early recognition and appropriate supportive therapy is vital for patient and, where possible, graft survival.

There have been few reported cases of cyanide toxicity following treatment with sodium nitroprusside. We report on the case of a paediatric patient who had received sodium nitroprusside for intractable hypertension in the post-operative period, resulting in cyanide toxicity. Treatment with sodium thiosulphate, sodium nitrate and haemodialysis resulted in the elimination of cyanide from the circulation. The patient made a full recovery with no neurological sequelae.

A previously well 12-year-old boy presented with a 1month history of polydipsia, polyuria, and lethargy. Over that period, he had been drinking at least 3 l of water daily, reported feeling thirsty, and needed to pass urine approximately every 30 min. His parents also reported that he had weight loss over the previous month with reduced appetite secondary to nausea. Of note, he had a long-standing history of drinking approximately 1 l of cow’s milk daily. He had no recent acute illnesses or fevers and reported no pain, discomfort, or respiratory distress. He had been treated with azathioprine for 3 years in the past for intractable eczema. His blood glucose level checked by his general practitioner was normal. Physical examination revealed significant bilateral inguinal lymphadenopathy and a 2-cm palpable liver edge. There were patches of dry skin attributed to previously diagnosed eczema. His cardiovascular, respiratory, neurological, ENT, and musculoskeletal examinations were otherwise unremarkable. There was an evident BCG scar. Vital signs were within normal limits. Laboratory investigations revealed acute renal impairment, hypercalcemia, and a mild transaminitis: urea 15.2 mmol/l, creatinine 149 mmol/l, serum calcium 3.38 mmol/l, ionized calcium 1.78 mmol/l, serum phosphate 1.42 mmol/l, sodium 139 mmol/l, potassium 3.7 mmol/l, AST 76 U/l, ALT 114 U/l, and lactate dehydrogenase 416 U/l. Serum intact parathyroid hormone levels were suppressed at