Frequent development of subclinical chronic antibody-mediated rejection within 1year after renal transplantation with pre-transplant positive donor-specific antibodies and negative CDC crossmatches.

Human immunology

PubMedID: 23792054

Yamanaga S, Watarai Y, Yamamoto T, Tsujita M, Hiramitsu T, Nanmoku K, Goto N, Takeda A, Morozumi K, Katayama A, Saji H, Uchida K, Kobayashi T. Frequent development of subclinical chronic antibody-mediated rejection within 1year after renal transplantation with pre-transplant positive donor-specific antibodies and negative CDC crossmatches. Hum Immunol. 2013;74(9):1111-8.
Although short-term graft survival has been improved by recent desensitization protocols including B cell depletion therapy, little is known about risk factors of chronic antibody-mediated rejection (CAMR) in HLA-incompatible (HLA-I) renal transplantation (RTx). Twenty-six HLA-I RTx with positive donor-specific antibodies (DSA) and negative T cell cytotoxic crossmatches were compared with 88 ABO-incompatible (ABO-I) and 207 ABO-identical/compatible (ABO-Id/C) RTx. The desensitization therapy consisted of mycophenolate mofetil, rituximab and double-filtration plasmapheresis. Protocol biopsies within 1year revealed subclinical CAMR in 36% of HLA-I, 5% of ABO-I and 3% of ABO-Id/C, although clinical acute AMR was observed in 8%, 3% and 1%, respectively. The incidence of CAMR was not different between class I and class II DSA. Most of class I DSA (94%) changed to negative 1year after RTx, whereas 77% of class II DSA remained positive. In addition, the remaining DRB±DQB DSA caused CAMR in 80% of patients, while DQB DSA alone did not. The progress of subclinical CAMR within 1year could not be circumvented by rituximab. Sustained class II (DRB±DQB) DSA detection after RTx may pose a potential risk for developing CAMR, but negative change in class I DSA could also elicit CAMR.