Abstract

Abstract: A 55‐year‐old female patient with chronic renal failure received an ABO‐incompatible secondary renal transplantation from her husband. She had positive pre‐operative flow panel reactive antibody reactivity to classes I and II. Donor‐specific antibody (DSA) was also positive in classes I and II. She was treated with rituximab, plasma exchange, and splenectomy before transplantation. The serum creatinine (sCr) level rose to 1.26 mg/dL on post‐operative day (POD) 17, and the episode graft biopsy specimen was diagnosed as mild acute vascular rejection. On POD 31, the protocol biopsy showed mild transplant glomerulitis and peritubular capillaritis (ptc2) with positive C4d, suggestive of antibody‐mediated rejection (AMR). She had cytomegalovirus (CMV) infection and was treated with ganciclovir. When the sCr rose to 1.7 mg/dL, two months post‐operatively, the episode biopsy showed mild AMR and no evidence of CMV infection. Since then, no clinical evidence of rejection has been observed, but protocol biopsy specimens obtained six and nine months postoperatively showed histologic findings suggestive of smoldering, persistent AMR. The patient was treated with deoxyspergualin and steroid pulse therapy after each protocol biopsy. Fourteen months after her operation, the protocol biopsy specimen revealed chronic allograft nephropathy with chronic rejection. It showed sclerosing vasculopathy with neomedia formation in the interlobular arteries and mild thickening of the peritubular capillary basement membrane with ptc1. DSA was not detected post‐operatively. With strategies using recently available immunosuppressive agents, the long‐term survival rate of renal grafts does not differ between ABO‐incompatible and ABO‐compatible cases. Anti‐human leukocyte antigen (HLA) antibody may have been the cause of smoldering AMR and consequent chronic rejection in this case. Further research is needed to devise a more successful desensitization regimen for organ transplantation in highly sensitized recipients.

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