An apparent paradoxical effect of pretransplant blood transfusions. Its association with decreased anti-HLA antibody formation following unsuccessful renal transplantation.
Many potential renal transplant recipients develop multispecific anti-HLA antibodies after a previous unsuccessful transplant. Therefore, it became important to analyze factors that could predispose to multispecific anti-HLA antibodies in the hope of preventing their occurrence because their presence hinders early retransplantation. In these studies, we elected to retrospectively analyze the impact of previous transfusions and the degree of HLA-A,B antigen mismatch on the development of these antibodies. Patients transplanted within the South Eastern Organ Procurement Foundation ( SEOPF ) after January 1977 were analyzed. All patients in these studies were immunosuppressed with prednisone and azothioprine . Antibodies to HLA antigens were determined in a complement-dependent microcytotoxicity assay utilizing recipient's sera and lymphocyte cell panels from random donors. Multispecificity of antibody was quantitated and expressed as the percentage of reactivity to lymphocyte panel (PRL). Only patients who lost their first cadaveric kidney allograft, and who, in addition, had a peak of less than 15% pretransplant and no prior pregnancies were analyzed. Peak posttransplant PRL had to be determined within 3 months after allograft failure. In the 146 patients with accurate transfusion data, it became evident that patients who received more than 5 pretransplant transfusions seldom developed greater than or equal to 50% PRL posttransplantation (P less than 0.001). Only 12% of patients receiving more than 5 pretransplant transfusions developed greater than or equal to 50% PRL, whereas 50% of patients with minimal pretransplant transfusions developed greater than or equal to 50% PRL. This protective effect of pretransplant transfusions was seen even in recipients receiving 3 and 4 HLA-A,B mismatched kidneys (P less than 0.01). The reason for this apparent protective effect is not clear from our data; it could be explained either on the basis of a selection process (i.e., exclusion of high responders pretransplant) or by suppression of the immune system. Nonetheless, these observations warrant attention, because the protective effect may be useful in preventing development of high PRL posttransplant in the event of a rejection.
D000918:Antibody Specificity; D000961:Antilymphocyte Serum; D001803:Blood Transfusion; D006084:Graft Rejection; D006680:HLA Antigens / Q000276:immunology*; D006650:Histocompatibility Testing; D006801:Humans; D007165:Immunosuppression Therapy; D016030:Kidney Transplantation; D011183:Postoperative Complications / Q000517:prevention & control; D011300:Preoperative Care; D065227:Transfusion Reaction
D000961:Antilymphocyte Serum; D006680:HLA Antigens