Acute Pancreatitis: A Rare Cause of Complement-Mediated Thrombotic Microangiopathy

Disruption of the complement regulatory system can provoke thrombotic microangiopathy (TMA), leading to clinical manifestations of generalized fatigue from hemolytic anemia, purpura caused by thrombocytopenia, and acute kidney injury from end-organ ischemia. This particular classification of TMA is known as complement-mediated thrombotic microangiopathy (CM-TMA). In CM-TMA, an inciting event such as infection, surgery, vaccination, or pregnancy triggers an inflammatory response resulting in the expression of inherited mutations or the development of autoantibodies against complement regulatory proteins, which leads to microangiopathic hemolytic anemia, thrombocytopenia, and direct damage to renal endothelial cells. The diverse etiologies of CM-TMA make diagnostic and therapeutic decisions a challenging endeavor. We encountered a young male patient who presented with significant lethargy and confusion. The initial diagnosis was consistent with systemic inflammatory response syndrome secondary to acute pancreatitis; however, the hospital course was complicated by subsequent acute renal failure, hemolytic anemia, and thrombocytopenia, likely indicating CM-TMA. The patient was successfully treated with plasma exchange therapy and eculizumab. We suspect that our patient likely developed CM-TMA from an episode of acute pancreatitis. Prompt diagnosis and early intervention are essential to improving morbidity and mortality. This is underscored by the development of monoclonal antibody therapy that directly targets the pathogenic complement proteins, which have been shown to improve renal disease outcomes.