Thrombotic Microangiopathy Associated With Concurrent Gemcitabine and Tacrolimus Exposure in a Patient With Pancreatic Adenocarcinoma and Cardiac Transplant

Drug-induced thrombotic microangiopathy (TMA) is an uncommon but potentially life-threatening condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, and end-organ injury.Diagnosis can be particularly challenging in patients where hallmark features can overlap with known comorbidities.We report a case of severe drug-induced TMA in a 75-year-old man with orthotopic heart transplantation on tacrolimus and pancreatic adenocarcinoma receiving gemcitabine presenting with acute kidney injury associated with acute thrombocytopenia, new tremors, and progressive generalized weakness.Subsequent evaluation revealed elevated serum lactate dehydrogenase (LDH), undetectable serum haptoglobin, and the presence of schistocytes on peripheral smear consistent with microangiopathic hemolytic anemia.Given recent exposure to both gemcitabine and tacrolimus, drug-induced TMA was suspected.Both tacrolimus and gemcitabine were discontinued, and empiric treatment with high-dose steroids and plasma exchange was initiated while awaiting a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) activity level testing.The hospital course was complicated by worsening renal function requiring initiation of hemodialysis and status epilepticus necessitating transfer to the intensive care unit.Following a normal ADAMTS13 activity level that effectively ruled out thrombotic thrombocytopenic purpura (TTP) and a lack of clinical improvement, corticosteroids and plasma exchange were discontinued and eculizumab was initiated.The patient gradually experienced neurologic improvement, hematologic recovery, and sufficient renal recovery to discontinue hemodialysis.This case highlights the diagnostic challenges that drug-induced TMA in medically complex patients present and the importance of early recognition and prompt intervention to limit irreversible endorgan damage.