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Sensitized patients remain a challenge for successful transplant. Virtual crossmatch is used to determine the presence or absence of donor-specific antibodies. A 60-year-old woman with a negative screening for panel-reactive antibodies (PRA) received an A*11, A*68 type kidney with a negative anti-human globulin/complement-dependent cytotoxicity (AHG-CDC) crossmatch. Her transplant course was complicated by delayed graft function, and she required hemodialysis. On day 8 after receiving the transplant, she had a kidney biopsy that showed features of antibody-mediated rejection/severe acute tubular necrosis, which was treated by plasmapheresis for 5 sessions and intravenous immunoglobulin (2 g/kg). Her serum level of creatinine decreased from 6.7 to 3.6 mg/dL (600-320 μmol/L). Panel-reactive antibody by Luminex was repeated and again was negative. Single-antigen detection was tried next. Surprisingly, A*11:02 came up positive with a mean fluorescence intensity of 9500. High-resolution donor HLA type was A*68:01 and A*11:01. A*11:02 is not part of the screening Luminex PRA whereas the 11:01 allele is. Serologically, HLA-A11 has 2 defined splits, A11.1 and A11.2, which encode A*11:01 and A*11:02, respectively. In this case, the A*11:02 antibody does not seem to be responsible for the increasing creatinine level. However, if the donor had been A*11:02, a humeral rejection would have occurred and been missed by a virtual crossmatch. Thus virtual crossmatch may not work at all times. Screening for PRA by single antigens is suggested even in PRA-negative cases, if only virtual crossmatch is to be used.
Sensitized patients remain a challenge for successful transplant. Virtual crossmatch is used to determine the presence or absence of donor-specific antibodies. A 60-year-old woman with a negative screening for panel-reactive antibodies (PRA) received an A*11, A*68 type kidney with a negative anti-human globulin/complement-dependent cytotoxicity (AHG-CDC) crossmatch. Her transplant course was complicated by delayed graft function, and she required hemodialysis. On day 8 after receiving the transplant, she had a kidney biopsy that showed features of antibody-mediated rejection/severe acute tubular necrosis, which was treated by plasmapheresis for 5 sessions and intravenous immunoglobulin (2 g/kg). Her serum level of creatinine decreased from 6.7 to 3.6 mg/dL (600-320 μmol/L). Panel-reactive antibody by Luminex was repeated and again was negative. Single-antigen detection was tried next. Surprisingly, A*11:02 came up positive with a mean fluorescence intensity of 9500. High-resolution donor HLA type was A*68:01 and A*11:01. A*11:02 is not part of the screening Luminex PRA whereas the 11:01 allele is. Serologically, HLA-A11 has 2 defined splits, A11.1 and A11.2, which encode A*11:01 and A*11:02, respectively. In this case, the A*11:02 antibody does not seem to be responsible for the increasing creatinine level. However, if the donor had been A*11:02, a humeral rejection would have occurred and been missed by a virtual crossmatch. Thus virtual crossmatch may not work at all times. Screening for PRA by single antigens is suggested even in PRA-negative cases, if only virtual crossmatch is to be used.
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