Shot in the Arm, Hit in the Kidney: A Case of Focal Thrombotic Microangiopathy Following Novavax COVID-19 Vaccination

Introduction: COVID-19 vaccines have greatly reduced SARS-CoV-2-related morbidity and mortality. However, rare but serious immune-mediated complications have emerged, including vaccine-induced immune thrombotic thrombocytopenia (VITT) and thrombotic microangiopathy (TMA). VITT is commonly reported with adenoviral vector vaccines but recent case reports suggest that protein subunit vaccines such as Novavax may also trigger immune responses leading to thrombotic/hematologic complications. Case Description: A previously healthy 58-year-old male developed low-grade fevers, weakness, arthralgia, 11-lb weight gain, one week after Novavax COVID-19 vaccine. An extensive infectious workup, including respiratory viral PCR, Hepatitis C, HIV, COVID-19, influenza, West Nile virus, and RSV, was negative. Autoimmune studies showed low C3 and C4 levels, and negative ANA, ANCA, and rheumatoid factor. His renal function continued to deteriorate, with BUN/cr peaking at 154/5.1 mg/dL with significant ansaraca. Renal biopsy revealed TMA While the initial CBC was normal, patient developed thrombocytopenia. Hematology was consulted, work up was consistent with immune thrombocytopenia (ITP), without evidence of microangiopathic hemolytic anemia with normal LDH, stable hemoglobin, no schistocytes. ADAMTS13 activity was within normal limits. Bone marrow biopsy ruled out hematologic malignancy. He was initiated on Eculuzimab along with hemodialysis. Subsequently he was treated with IVIG, Rituximab, steroids, for ITP. His renal function improved prior to stabilization of platelets allowing dialysis cessation after 3 months. Renal function has been stable on maintainence dose of eculuzimab and platelets maintained on mycophenolate and avatrombopag. Discussion: This case highlights a rare but serious immune-mediated syndrome after Novavax COVID-19 vaccination The absence of ADAMTS13 deficiency and negative autoimmune serologies pointed toward a complement-mediated TMA rather than thrombotic thrombocytopenic purpura (TTP). Complement dysregulation causes endothelial injury in complement mediated TMA, rescue therapy with eculizumab (anti-C5 monoclonal antibody) initiated early helps in renal survival and treatment is generally recommended usually for 6–12 months. Early recognition, comprehensive evaluation, and multidisciplinary treatment approach are critical to the patient’s recovery.