Influenza A–Associated Thrombotic Microangiopathy With Normal a Disintegrin and Metalloproteinase With Thrombospondin Type 1 Motif 13 (ADAMTS13) in a Young Male Patient: A Case Report

Thrombotic microangiopathy (TMA) is a life-threatening syndrome characterized by microangiopathic hemolytic anemia, thrombocytopenia, and end-organ injury resulting from widespread microvascular thrombosis. It encompasses several entities, including thrombotic thrombocytopenic purpura (TTP), atypical hemolytic uremic syndrome (aHUS), and secondary forms triggered by infections, medications, or systemic disease. Viral infections, including influenza A, have been increasingly recognized as rare triggers of secondary TMA, through endothelial injury and immune dysregulation, even in the absence of severe a disintegrin and metalloproteinase with thrombospondin type 1 motif 13 (ADAMTS13) deficiency. We report a case of a 21-year-old male patient who presented with fever, productive cough, and cola-colored urine following a positive influenza A antigen test. He was found to have severe thrombocytopenia, microangiopathic hemolytic anemia with schistocytes on peripheral smear, markedly elevated lactate dehydrogenase, acute kidney injury, and concurrent rhabdomyolysis. ADAMTS13 activity was 0.8 IU/mL (equivalent to 80% activity), within the normal range, and consistent with secondary influenza A-triggered TMA. The patient was treated with therapeutic plasma exchange and high-dose intravenous methylprednisolone, achieving full hematological recovery. This case highlights the importance of recognizing influenza A as a trigger of secondary TMA with a TTP-like phenotype despite normal ADAMTS13 activity, and underscores the critical role of early empiric plasma exchange as a life-saving intervention.