A Case of Severe Thrombotic Microangiopathy from Tacrolimus in a Kidney Transplant Recipient

Introduction: Calcineurin inhibitors are considered first-line medications for maintenance immunosuppression in kidney transplant patients. However, tacrolimus has the potential to induce thrombotic microangiopathy (TMA) rarely. Here, we report a case of tacrolimus-induced TMA in the early post-transplant period. Case Description: A 47-year-old male with end-stage kidney disease due to diabetes mellitus and hypertension underwent a deceased donor kidney transplant (DBD donor, KDPI 52%, cold ischemia time 20 hours). Induction immunosuppression included thymoglobulin (4.5 mg/kg) and methylprednisolone. Maintenance immunosuppression with tacrolimus and mycophenolic acid was initiated on postoperative day (POD) 1. On POD 4, the patient developed acute anemia and thrombocytopenia (Hb 10.1 → 6.8 g/dL; platelets 254,000 → 24,000/µL). Laboratory findings revealed schistocytes on peripheral smear, elevated LDH (665 U/L), indirect hyperbilirubinemia (1.6 mg/dL), low haptoglobin (2 mg/dL), and a rise in serum creatinine (8.8 → 11.3 mg/dL) with normal PT/aPTT—findings consistent with TMA. Complement panel was negative. Tacrolimus was suspected as the culprit and was discontinued given such an early onset post-transplant TMA, cyclosporine was initiated. The patient experienced delayed graft function requiring one hemodialysis session and received multiple transfusions for anemia and thrombocytopenia. By day five post-tacrolimus withdrawal, hemoglobin and platelet levels began to recover, with normalization of haptoglobin and bilirubin. Renal function gradually improved. At six-month follow-up, serum creatinine remained stable between 2.2–2.5 mg/dL with an eGFR of ~32 mL/min. Discussion: Drug-induced TMA is thought to result from either immune-mediated reaction to the drug or toxic drug doses. Management centers on prompt withdrawal of the offending agent. This case highlights the importance of early recognition and intervention, as discontinuation of tacrolimus alone led to significant improvement. In refractory cases, additional therapies such as for plasma exchange, IVIG in combination with steroids, rituximab, or eculizumab may be necessary. While de novo TMA post-transplant is rare, it is a serious complication associated with poor graft outcomes, even after resolution.