ArticleThe American journal of case reports2026
Tacrolimus-Induced Thrombotic Microangiopathy in a Kidney Transplant Recipient After Treatment for Acute Allograft Rejection.
Article in The American journal of case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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