A 43-yr-old woman with end-stage renal disease caused by lupus nephritis received living kidney transplantation with ABO minor mismatch from her mother. Urine output decreased rapidly from fifth postoperative day, and serum creatinine (sCr) concentration increased rapidly. The clinical diagnosis was antibody-mediated rejection. The patient was treated with pulse methylprednisolone, plasma exchange (PEX), and OKT3. A graft biopsy revealed vascular rejection with linear C4d deposition on peritubular capillary (PTC). She was treated with additional PEX and intravenous cyclophosphamide, which improved urine output and resulted in a gradual decrease in sCr. She subsequently developed frequent episodes of acute rejection (AR) with a rise in sCr. Repeated graft biopsies revealed acute T-cell-mediated rejection with progressive interstitial fibrosis and tubular atrophy. Severe peritubular capillaritis with mononuclear infiltrates were present, but C4d deposition on PTC was persistently negative or weak. Flow-cytometric panel reactive antibody performed retrospectively revealed both donor- and non-donor-specific HLA antibodies, which were persistently present after the treatment of the first AR. We added rituximab to the treatment of AR, but she developed cytomegalovirus enteritis, and eventually hemodialysis was induced again 45months after the transplantation. Recent flow-cytometry-based antibody detection methods are useful even in cases lacking diffuse and strong C4d deposition on PTC.
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