Histocompatibility testing in human renal allografts. I. Evidence for a strong and a weak HL-A sublocus in recipients of allografts from living related donors

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THE significant correlation of histocompatibility typing with the clinical status of patients who received renal allografts from living related donors has been demonstrated for sibling-sibling and for parent-child pairs.1–3 Those who did not show such a correlation constituted two major groups of patients: those mismatched recipients whose allografts retained good function, and those matched recipients whose allografts failed. These discrepancies between histocompatibility testing and renal allograft survival may have been attributable to several major factors: (1) differences in strength of histocompatibility antigens, (2) effects of antigenic combinations, (3) differences in response of various hosts to the same histocompatibility antigens, (4) inadequacies of leukocyte typing sera for detecting HL-A histocompatibility antigens, (5) presence of other histocompatibility loci in addition to the HL-A locus.

By using well-defined leukocyte antisera capable of detecting 13 HL-A antigens and thus minimizing the fourth factor, we attempted to gain information in regard to the effect of the other factors, particularly the relative strength of histocompatibility antigens. Because this study was retrospective, there was a bias against finding a strong histocompatibility antigen, since those patients with such a mismatch may have already died. Of equal importance, however, was the detection of weak antigens most apparent in those mismatched recipients with prolonged allograft survival. This latter group of patients has accounted for the majority of discrepancies between tissue typing and clinical status.1

Patients and methods

Patients. Of 31 patients at the Cleveland Clinic Hospital who each received a renal allograft from a living related donor, maintained allograft function . . .



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