Tacrolimus-Induced Thrombotic Microangiopathy in a Kidney Transplant Recipient After Treatment for Acute Allograft Rejection.

BACKGROUND Tacrolimus is widely used in solid-organ transplantation but has been associated with thrombotic microangiopathy (TMA), a rare yet potentially life-threatening complication that can result in graft dysfunction or loss. The reported incidence ranges from 1% to 4.7% in transplant recipients. Diagnosis is challenging because clinical manifestations overlap with rejection, infection, and other secondary causes, making timely recognition critical. CASE REPORT A 48-year-old kidney transplant recipient developed anemia, thrombocytopenia, and acute kidney injury 23 days after initiating tacrolimus for acute T-cell-mediated rejection. The patient also experienced neurologic and gastrointestinal symptoms. Microangiopathic hemolytic anemia was confirmed by the presence of schistocytes on peripheral smear, elevated lactate dehydrogenase, and low haptoglobin; gastrointestinal bleeding was excluded. Comprehensive diagnostic evaluation-including a disintegrin and metalloproteinase with thrombospondin type 1 motif, member 13 (ADAMTS13) activity, complement studies, coagulation testing, and infectious screening-excluded alternative etiologies of TMA. Although tacrolimus trough concentrations remained within the therapeutic range, the temporal association supported tacrolimus-induced TMA. Tacrolimus was promptly discontinued, resulting in complete hematologic and renal recovery within 10 days. During follow-up, tacrolimus reintroduction for refractory rejection led to recurrence of hemolytic anemia and thrombocytopenia, which again resolved after drug withdrawal. This dechallenge-rechallenge pattern yielded a Naranjo score of 9, indicating a definite adverse drug reaction. CONCLUSIONS This case highlights the importance of early recognition and systematic exclusion of competing etiologies when evaluating suspected drug-induced TMA. Distinguishing tacrolimus toxicity from rejection-related graft dysfunction is essential-prompt discontinuation of the offending agent can prevent irreversible kidney injury and graft loss.