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Atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) that can result in end-stage renal disease. Patients with aHUS often have predisposing dysfunction in the complement pathway, and continuous activation of complement proteins can be triggered after transplantation. Here, we report the first successful case of aHUS treatment in a kidney transplant recipient with early use of a C5 inhibitor, eculizumab, in South Korea. The patient was a 32-year-old man, and the donor was his 60-year-old mother. The graft showed immediate good function. On postoperative day (POD) 3, the clinical diagnosis of TMA was made. Persistent renal dysfunction despite 10 plasma exchange (PE) sessions prompted eculizumab treatment on POD 18 under suspicion of aHUS. Next-generation sequencing reported gene mutations classified as variants of unknown significance in coagulation-associated genes. The patient was discharged after three doses of eculizumab with serum creatinine of 1.82 mg/dL. In total, 16 doses of eculizumab were administered. At the last follow-up, 21 months after eculizumab discontinuation, the graft was well functioning. De novo TMA after kidney transplantation can be caused by sustained activation of the complement pathway, and early eculizumab treatment appears important in the successful treatment of aHUS refractory to PE., Competing Interests: Conflict of Interest No potential conflict of interest relevant to this article was reported., (Copyright © 2023 The Korean Society for Transplantation.)

Malakoplakia is a rare, granulomatous disease that usually affects immunocompromised individuals and is generally associated with poor graft and patient survival. We present a case of renal malakoplakia after kidney transplantation (KT). A 33-year-old female patient with chronic kidney disease underwent living-donor KT at Severance Hospital. The patient was administered 375 mg/m 2 rituximab due to high panel reactive antibodies. Immunosuppression was initiated with 1.5 mg/kg anti-thymocyte globulin and intravenous methylprednisolone and maintained with tacrolimus, oral methylprednisolone, and mycophenolate mofetil (MMF). Six months after KT, the patient was hospitalized for a urinary tract infection with an elevated serum creatinine level of 3.14 mg/dL. Renal biopsy revealed malakoplakia involving the renal parenchyma. Upon this diagnosis, the dose of tacrolimus was reduced and MMF was stopped. Fluoroquinolone was used for 16 days, and the trimethoprim/sulfamethoxazole dose was doubled for 6 days. The patient was hospitalized for 3 weeks and closely observed during outpatient visits. Follow-up ultrasonography revealed mass-like lesions of renal malakoplakia, which disappeared 5 months after diagnosis. The serum creatinine level decreased to 1.29 mg/dL 28 months after diagnosis. Our results suggest that renal malakoplakia can be successfully treated by the reduction of immunosuppression and sustained antimicrobial therapy., Competing Interests: Conflict of Interest No potential conflicts of interest relevant to this article are reported., (© 2022 The Korean Society for Transplantation.)