thrombotic microangiopathy; This literature marketed report has been received from the authors of a published literature article, titled as stated below, and refers to a 5-month-old female patient who was treated with onasemnogene abeparvovec (ZOLGENSMA) for spinal muscular atrophy (SMA). On an unknown date, four days before onasemnogene abeparvovec (ZOLGENSMA) dosing, the patient was hospitalized for aspiration pneumonia. Her sputum culture grew Proteus and Acinetobacter species. On an unknown date, the patient received onasemnogene abeparvovec (ZOLGENSMA), one-time intravenous infusion administered concomitantly with corticosteroid (prednisolone 1 day prior to the infusion, and for a minimum of 30 days following treatment). On an unknown date, three days after onasemnogene abeparvovec (ZOLGENSMA) dosing, the patient developed second event of pneumonia. On an unknown date, six days after onasemnogene abeparvovec (ZOLGENSMA) dosing, the patient was vaccinated with a dose of haemophilus b conjugate vaccine (meningococcal protein conjugate) (manufacturer unknown) (exact dose, dose#, route of administration, lot# and expiration date were not reported), concomitantly with an unspecified influenza virus vaccine live (exact dose, dose#, route of administration, lot# and expiration date were not reported) and pneumococcal 4 6b 9v 14 18c 19f 23f conj vaccine (crm197) (PREVNAR) (exact dose, dose#, route of administration, lot# and expiration date were not reported), all for prophylaxis. On an unknown date, seven days after onasemnogene abeparvovec (ZOLGENSMA) dosing, the patient developed hypertension and decreased urine output as first symptoms of thrombotic microangiopathy (TMA). TMA developed with hemolytic anemia, hematuria, proteinuria, leukocytosis, thrombocytopenia, and severe hypertension. Renal ultrasound scan indicated diffuse increase in cortical echogenicity bilaterally. Functional TMA panel indicated evidence of complement pathway activation with no autoantibodies or abnormal complement components (low complement C4 (0.07 g/L), and normal complement C3 (1.1 g/L), complement Factor H (CFH) (369 mg/L), complement Factor I (34 mg/L), negative complement factor H autoantibody (CFHAb) (less than 50 AU), complement total (CH50) (160 U eq/mL), high soluble complex C3b-9 (0.9 mg/L)). Genetic evaluation was not performed. Other laboratory evidence of TMA included: hemoglobin 7 g/dL (Nadir) (on day 7 after onasemnogene abeparvovec (ZOLGENSMA) dosing; baseline: 10.3 g/dL); platelet count 17 k/micro-l (Nadir) (baseline: 503 k/micro-l); creatinine 0.7 mg/dL (peak) (baseline: 0.1 mg/dL); lactate dehydrogenase (LDH) 4208 U/L (peak). There was protein and blood present in the urine. Prothrombin time (PT), partial thromboplastin time (PTT) and international normalized ratio (INR) were normal. Stool and urine cultures were negative. ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) assay was normal. The patient was treated with packed red blood cell (PRBC) and platelets transfusions, glucocorticoids, plasmapheresis, diuretic for fluid overload, antihypertensives. The features of TMA resolved within 2 weeks, except hypertension, which continued to persist 1 year later. The authors of the article considered TMA to be drug-induced by onasemnogene abeparvovec (ZOLGENSMA), resulting from immune-mediated etiology. Additionally, TMA was related to concurrent infection with encapsulated bacteria and vaccine exposure to haemophilus b conjugate vaccine (meningococcal protein conjugate) (manufacturer unknown), unspecified influenza virus vaccine live and pneumococcal 4 6b 9v 14 18c 19f 23f conj vaccine (crm197) (PREVNAR).  Upon internal review, TMA was considered medically significant.  A copy of the published article is attached as further documentation of patient's experience.