The impairment of graft function by antibody-mediated humoral rejection has received widespread attention from the international transplant community. The results of an international multicenter prospective study showed that among 2,278 kidney transplant recipients, the 1-year graft loss in 1-year postoperative period was 3.3% in 1,778 patients who did not have HLA antibodies, whereas the 1-year graft loss in 500 patients who developed HLA antibodies was 6.6%, which suggests that the presence of HLA antibodies plays an important role in graft loss. In addition, Mauiyyedi et al. confirmed the morphological characterization of chronic rejection: 61% of patients with glomerulopathy (TG) and/or chronic graft arteriopathy (arterial endothelial fibrosis with endothelial mononuclear cells and/or foam cell B outgrowths) showed C4d deposition in the peritubular capillary wall (PTC), while 88% of C4d-positive chronic rejection patients had the presence of donor-specific antibodies. specific antibodies. In view of the conclusive evidence of the close correlation between antibody-mediated humoral rejection and impaired graft function, the 2003 Banff Conference formally included C4d deposition on the peritubular capillary wall (PTC) in the diagnostic criteria for antibody-mediated humoral rejection and emphasized that C4d deposition is the strongest in situ evidence of active humoral rejection. It is known that humoral rejection is mainly mediated by specific antibodies against donor antigens, so effective prevention and inhibition of the production of donor-specific antibodies is the key to reducing humoral rejection: 1, preoperative emphasis on donor-recipient HLA mapping, according to cross-reactivity group or amino acid residue mapping strategy to select acceptable mismatched antigens and/or less mismatched antigens, and effective prevention of the production of donor-specific HLA antibodies ; 2. Adjustment and optimization of immunosuppression protocols. We observed that 36 patients with preoperative positive population reactive antibodies (PRA), who received the triple immunosuppressive therapy of tacrolimus + primaquine + prednisone after renal transplantation, turned negative for PRA after 6-12 months, and another 12 patients who were highly sensitized preoperatively (PRA>50%) had significantly lower PRA levels postoperatively. Therefore, for PRA-positive patients, we recommend a triple immunosuppressive treatment regimen of tacrolimus + primaquine + prednisone; 3. Intravenous infusion of human CD20 monoclonal antibody (Rituximab) to inhibit the activity of B-lymphocytes in vivo; 4. Intravenous infusion of immunoglobulin (IVIG), or immunoadsorbent (IA) and plasma exchange (PE) therapy to remove donor-specific antibodies produced in vivo, and reduce humoral IVIG or immunosorbent (IA) and plasma exchange (PE) treatment to remove the donor-specific antibodies produced in the body and reduce the damage to the graft caused by humoral rejection.