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13 May 2026 : Case report  Taiwan

[In Press] Tacrolimus-Induced Thrombotic Microangiopathy in a Kidney Transplant Recipient After Treatment for Acute Allograft Rejection

Unusual clinical course, Challenging differential diagnosis, Unusual or unexpected effect of treatment, Diagnostic / therapeutic accidents, Adverse events of drug therapy, Clinical situation which can not be reproduced for ethical reasons

Yen-Hao Liao1ABDEF, Ming-Yi Huang1DF

DOI: 10.12659/AJCR.953247

Am J Case Rep In Press; DOI: 10.12659/AJCR.953247  

Available online: 2026-05-13, In Press, Corrected Proof

Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule

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.

Keywords: Kidney Transplantation; Tacrolimus; Thrombotic Microangiopathies

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

Am J Case Rep In Press; DOI: 10.12659/AJCR.953247  

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923