Clinical hyperacute kidney rejection (HKR) was first described by KissmyerNeilsen et al. in 1966 [I 11. Starzl et al. described a high rate of HKR in transplants done across major ABO incompatibilities [ 181. Williams and co-workers demonstrated the relationship of this phenomenon to humoral antibodies directed against donor kidney antigens [26], and Terasaki and Singal showed the relationship of HKR to a positive donor-recipient cross match [ 191. With the development of more sensitive cross-matching techniques, the incidence of HKR has declined markedly [19] although HKR still continues to occur in l12% of renal transplants. This rejection phenomenon is vexing because of a rather high rate of occurrence in presensitized patients and in patients requiring secondary transplantation [23]. In addition, there is currently no effective treatment for HKR. At least one group has attempted unsuccessfully to prevent HKR in sensitized patients using infusions of F(ab’), antibodies and citrate pretreatment [7]. HKR is known to involve a complementfixing antibody [ 1 l] whereas recent work has suggested that some antibodies which do not fix complement may produce a state of enhancement favoring allograft prolongation [27]. This work suggests conceptually that HKR might be abrogated and a system