severe hypertension; Thrombotic Microangiopathy; hemolytic anemia; thrombocytopenia; hematuria; proteinuria; leukocytosis; This case was reported in a literature article and described the occurrence of thrombotic microangiopathy in a 5-month-old female patient who received Flu unspecified (Influenza vaccine) for prophylaxis.   Co-suspect products included Hib UNK (Hib vaccine) (batch number UNK, expiry date unknown) for prophylaxis and PNEUMOCOCCAL VACCINE (PREVENAR) (batch number UNK, expiry date unknown) for prophylaxis.   Concurrent medical conditions included spinal muscular atrophy (treated with Onasemnogene abeparvovec) and pneumonia. Concomitant products included prednisolone.   On an unknown date, the patient received Influenza vaccine, Hib vaccine and PREVENAR. On an unknown date, 1 day after receiving Influenza vaccine and Hib vaccine, the patient experienced thrombotic microangiopathy (serious criteria GSK medically significant), hemolytic anemia (serious criteria GSK medically significant), thrombocytopenia (serious criteria GSK medically significant), hematuria, proteinuria, leukocytosis and hypertension. The patient was treated with operations and procedures (Plasmapheresis (Nos)), red blood cells (Red Blood Cell), platelets, human blood (Platelet Transfusion), glucocorticoids nos (Glucocorticoids), diuretics nos (Diuretic) and antihypertensives nos (Antihypertensives). On an unknown date, the outcome of the thrombotic microangiopathy, hemolytic anemia, thrombocytopenia, hematuria, proteinuria and leukocytosis were recovered/resolved and the outcome of the hypertension was unknown.   It was unknown if the reporter considered the thrombotic microangiopathy, hemolytic anemia, thrombocytopenia, hematuria, proteinuria, leukocytosis and hypertension to be related to Influenza vaccine and Hib vaccine.  Additional details were provided as follows: This case was reported in a literature article and described the occurrence of Thrombotic Microangiopathy (TMA), in a 5-month-old female patient, who was vaccinated with Unspecified Influenza vaccine; Unspecified Hemophilus influenza B (Hib) vaccine (manufacturer unknown for both) for prophylaxis.  The patient had Spinal Muscular Atrophy. The patient received prednisolone 1 day prior to and for a minimum of 30 days following treatment with 1.1X10E14 vg/kg of onasemnogene abeparvovec. The patient was treated with onasemnogene abeparvovec while hospitalized and undergoing treatment for aspiration pneumonia. Second event of pneumonia 3 d after dosing. The patient had another episode of pneumonia 3 days after onasemnogene infusion. Four days before dosing, the patient sputum culture grew Proteus and Acinetobacter species (Aspiration pneumonia 4 d before dosing; (Acinetobacter baumannii and Pasteurella). The patient weight at onasemnogene abeparvovec dosing was 6.5 kg. The patient did not have Nusinersen (most recent dose). The source of report was registry of patients with spinal muscular atrophy receiving disease-modifying therapies. No information on patient family history concomitant medication was reported.   On an unknown date, 6 days after receiving onasemnogene abeparvovec, the patient received Unspecified Influenza vaccine; Unspecified Hemophilus influenza B (Hib) vaccine. The patient also received Prevenar vaccine (administration site unspecified, dose number unknown; batch number not provided for all).  The age at vaccination was not provided but it could be between 4 months or 5 months at the time of vaccination.  On an unspecified date, seven days after onasemnogene infusion, 1 day after vaccination, the patient developed TMA with hemolytic anemia, hematuria, proteinuria, leukocytosis, thrombocytopenia, and severe hypertension. Renal ultrasound scan indicated diffuse increase in cortical echogenicity bilaterally. Laboratory evidence of TMA (baseline and following onasemnogene abeparvovec): Haemoglobin: Baseline: 10.3 g/dL, Nadir: 7 g/dL (day 7); platelet: Baseline: 503 k/mcL, Nadir: 17 k/mcL; Creatining: Baseline: 0.1 mg/dL, Peak: 0.7 mg/dL; Lactate dehydrogenase (LDH): Peak: 4208 U/L. Urinalysis showed Protein and blood. Prothrombin time (PT), Partial thromboplastin time (PTT) and International normalized ratio (INR) were normal. Acute complement pathway investigations (classic/alternative) at presentation of TMA: Complement (C3): 1.1 g/L (ref 0.9-1.8) ; Complement (C4): 0.07 (ref 0.15-0.57) ; Bb fragment concentration: 3.8 mg/L (ref less than 2.2); Soluble C5b-9: 0.9 mg/L (ref less than 0.3); CH50: 160 U eq/mL (ref more than70); FH autoantibody less than 50 AU (ref less than 200 AU); Factor B: 32.3 mg/dL (ref 22-50); Factor H: 369 mg/L (ref 180-420); Factor I: 34 mg/L (ref 16-40). Investigations concerning potential predisposition factors (hereditary or acquired): Functional complement assay with low C4, and normal C3, CFH, I, neg anti-complement factor H autoantibody (CFHAb), CH50, high C3b-9 (SMAC), a disintegrin and metalloproteinase with thrombospondin motifs 13 (ADAMTS13) normal. No genetic testing completed. Stool and urine cultures negative. The features of TMA resolved within 2 weeks following plasmapheresis, except hypertension, which continued to persist 1 year later. Functional TMA panel indicated evidence of complement pathway activation with no autoantibodies or abnormal complement components. Genetic evaluation was not performed.  Treatment included packed red blood cell (PRBC) and platelet transfusions, glucocorticoids, plasmapheresis, diuretic for fluid overload, antihypertensives.  Outcome from the time of diagnosis: Recovered (2 week) with persistent hypertension.  The authors commented "We have reported 3 children with SMA who developed TMA following onasemnogene abeparvovec therapy. These cases share several similarities. TMA developed approximately 1 week following onasemnogene abeparvovec infusion, 2 of the 3 children suffered from vomiting, 2 of the 3 had previous exposure to nusinersen, and 2 had infections with encapsulated organisms. Patient 1 had an infection preceding TMA with a new infection shortly after infusion. Drug-induced TMA is theorized to result from immune-mediated reactions or a dose-/duration-dependent direct toxic effect. Differentiating criteria include early temporal association with drug administration in the former as opposed to a delayed onset from a cumulative exposure in the latter. Our 3 patients developed TMA approximately 1 week after administration, suggesting an immune-mediated etiology. Other causes and presentations of TMA include hemolytic uremic syndrome resulting from shiga toxin-positive E coli; thrombotic thrombocytopenic purpura resulting from a reduction of ADAMTS13, the protease that cleaves von Willebrand factor (vWF); hereditary deficiencies in regulation of coagulation or alternative complement pathways; and a wide variety of infectious pathogens, including encapsulated organisms. In addition to exposure to onasemnogene abeparvovec, each of the 3 patients had contributory factors that could be putatively associated with TMA. Potential triggering factors include concurrent infection with encapsulated bacteria and recent vaccine exposure. It is unknown what additional risks to onasemnogene abeparvovec, if any, previous exposure to nusinersen confers. If thrombocytopenia is present and there is a clinical suspicion of TMA, further evaluation including hemoglobin hemoglobin and testing for hemolysis and renal dysfunction (including urinalysis) also should be obtained. Early recognition of TMA is imperative, as TMA may require therapeutic intervention such as plasmapheresis, dialysis, or pharmacotherapy, to lessen associated morbidity and mortality".