Abstract

Gerald S Lipshutz1, Elaine F Reed2, Phuong-Chi Pham3, Jeffrey M Miller4, Jennifer S Singer5, Gabriel M Danovitch6, Alan H Wilkinson6, Dean W Wallace7, Suzanne McGuire6, Phuong-Truc Pham8, Phuong-Thu Pham61Department of Surgery, Kidney and Pancreas Transplant Program, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 2Department of Pathology and Laboratory Medicine-Immunogenetics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 3Department of Medicine, Nephrology Division, UCLA-Olive View Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 4Department of Medicine, Hematology Oncology Division, UCLA-Olive View Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 5Department of Surgery and Urology, Kidney and Pancreas Transplant Program, 6Department of Medicine, Nephrology Division, Kidney and Pancreas Transplant Program, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 7Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 8Department of Science, Penn State University, Worthington-Scranton, Dunmore, PA, USA: Over the past decade ABO incompatible transplantation has emerged as an important potential source for increasing living kidney transplantation in selected transplant centers. Early reports suggest that patients who have elevated serum anti-blood group antibody titers before transplantation and a rebound antibody production after antibody removal may be at high immunological risk. With currently available immune modulation protocols and immunosuppressive therapy, excellent short- and long-term patient and graft survival rates have been achieved even in those with high anti-A/B antibody titers before plasmapheresis or immunoadsorption. Nonetheless, acute infection with an organism possessing surface markers analogous to blood group antigens such as carbohydrate structures on the surface of bacterial cell wall occurring before the firm establishment of accommodation can trigger the onset of acute antibody-mediated rejection. We herein report a case of delayed hyperacute rejection in an A1 to O, ABO incompatible transplant recipient following an episode of Clostridium difficile infection.Keywords: ABO incompatible transplantation, delayed hyperacute rejection, kidney transplantation, Clostridium difficile infection