Atypical hemolytic uremic syndrome (aHUS) is an infrequently encountered complement-mediated thrombotic microangiopathy (TMA) usually associated with germline variants in genes of the complement system. Clinical findings of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury (AKI) with severe hypertension arise due to aberrant complement protein activation in the circulation and significant endothelial damage. Transplant-associated thrombotic microangiopathy has been increasingly recognized after high dose carboplatin, etoposide, and melphalan-chemotherapy followed by autologous hematopoietic stem cell rescue for treatment of children with neuroblastoma (NB). We report the case of a 13-month-old boy with metastatic neuroblastoma who developed aHUS during the first cycle of induction chemotherapy. Germline testing revealed a Complement factor H (CFH) gene mutation, Cys357Arg, which is currently classified as a variant of uncertain significance (VUS), although likely pathogenic based on molecular modeling as well as this patient’s clinical presentation. The patient has been successfully managed with complement blockade therapy with no recurrence of disease. We review presentations of neuroblastoma with hypertension, along with AKI and thrombocytopenia, to raise awareness about the potential for aHUS in patients with newly diagnosed NB.

Children with cancer who develop fever in the setting of chemotherapy-induced neutropenia are treated empirically for bacteremia. Viral etiologies are most common and there remains no consensus about anticipatory guidance that should be provided to patients regarding community-acquired infections. Using COVID-19 positivity as a surrogate for a community acquired infectious exposure, we performed a retrospective chart review of pediatric oncology patients diagnosed with COVID-19 during the Omicron (B.1.1.529) surge at The Children’s Hospital at Montefiore. No patients in our cohort developed bacteremia, or serious respiratory illness. Future studies will aid in understanding the relationship between bacteremia and community acquired infections in order to provide evidence-based recommendations about environmental exposures and guide optimal care for our patients.

Posttransplant lymphoproliferative disorder is a rare but well-known complication in solid organ or hematopoietic transplant recipients secondary to immunosuppression. It can range from a cellular hyperplasia to a classic lymphoma. We describe a case of a nine-year-old male with Barth syndrome and a history of cardiac transplantation who developed plasmacytoid EBV-negative PTLD, an extremely rare entity in the pediatric population, and the evolvement of his PTLD to a more aggressive plasma cell neoplasm.