Lewis antibodies and renal transplantation

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Kidney cells biosynthesize Lewis antigens [721]. The role of cytotoxic Lewis antibodies in kidney graft survival is controversial. In 1978, from a retrospective study of 255 kidney transplant recipients, Oriol et al. [793] found that 2-year graft survival rates were significantly lower in Le(a-b-) recipients than in Le-

positive recipients, leading to the proposal that antigens of the Lewis system represented histocompatabil-ity antigens in renal transplantation. This was supported by other retrospective studies [794-796] and by a prospective study [797] in which Lewis-identical donor-recipient pairs were shown to have better graft survival than Lewis-incompatible pairs. Further support came from individual cases in which Lewis antibodies were implicated as the possible cause of renal transplant rejection [798]. Spitalnik et al. [799], by their highly sensitive kinetic enzyme-linked immunosorbent assay, revealed the presence of anti-Lea in all of eight Le(a-b-) patients with failed renal grafts, but not in the single Le(a-b-) recipient of an Le(a-b-) graft. Most of these antibodies could not be detected by haemagglutination. In two other prospective studies and one retrospective study [800-802], however, no significant difference in survival between Lewis-matched and Lewis-mismatched donor-recipient pairs was detected, although Le(a-b-) patients appeared to be at higher risk of graft failure when receiving HLA mismatched kidneys. These data led to the recommendation that kidneys should not be selected for engraftment on the basis of Lewis phenotype [801].

Anti-Lea, presumably of graft origin, has been blamed for renal failure in bone marrow transplant recipients [729,803]. Autoanti-LebH in an Le(a-b+) patient who had received two kidney transplants that had both been rapidly rejected, agglutinated the patient's own red cells and was inhibited by his own saliva [798,804].

2.19 Other antigens associated with Lewis

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