6 renal transplant patients, seen at the Mayo Clinic between July 1982 and April 1983, received Minnesota antilymphoblast globulin (MALG) for treatment of allograft rejection and demonstrated warm-acting 'auto'-antibodies during such therapy. These antibodies represented xenogeneic reactivity in equine MALG, rather than the products of patient-derived immune responses, since they were not detected before or after the period of therapy with this immunosuppressive agent in any of the 6 cases. They interfered with crossmatch procedures for red cell transfusion, and were only variably removed by autoabsorption techniques. Heat treatment of sera containing MALG-related red cell antibodies was ineffective in abrogating their reactivity and also compromised the reactivity of some red cell alloantibodies which were tested as controls. Transfusion of 'least-incompatible' red blood cells had no adverse effects in 2 cases where it was necessitated by clinical circumstances, despite an inability to obtain suitable serological samples for crossmatching.

A 79-year-old woman with a diagnosis of lower gastrointestinal bleeding was found to have a complementdependent anti-Jk sup(a) i n her serum. The anti -Jk sup(a) was evaluated by the antiglobulin technique with polyspecific, anti-C3, and anti-IgG antihuman globulin (AHG). A variety of Sensitization and detection methods were used, including the prewarmed saline technique, enzyme treatment of test cells, a low-ionic additive solution (LISS), 22 percent albumin, Polybrcnc, and an increased scrum/cell ratio. The anti -Jk sup(a) was detected only when polyspecific AHG and anti-C3 were used compared to anti-IgG, regardless of the selected enhancement technique. Anti-C3 gave weaker reactions than polyspecific AHG. IgG subclassing was inconclusive. The anti -Jk sup(a) was not detected when plasma was substituted for serum. The use of polyspecific versus IgG AHG in prctrmsfusion testing is discussed. In 1951, Allen et al . sup( 1) reported the first case of hemolytic disease of the newborn (HDN) associated with anti-Jk sup(a). Since then, other cases have been reported in which anti-Jk sup(a) caused severe HDN sup(2) or, in one case, caused no clinical symptoms. sup(3) However, the evidence that anti-Jk sup(a) 4-6 and -Jk sup(b) 7 cause acute and delayed hemolytic transfusion reactions is well documented.Kidd system antibodies are often difficult to identify, as they are rarely potent, can show a dosage effect by reacting more strongly with Jk(a+b-) than with Jk(a + b +) cells, and frequently become nondetectable

6 renal transplant patients, seen at the Mayo Clinic between July 1982 and April 1983, received Minnesota antilymphoblast globulin (MALG) for treatment of allograft rejection and demonstrated warm-acting ‘auto’-antibodies during such therapy. These antibodies represented xenogeneic reactivity in equine MALG, rather than the products of patient-derived immune responses, since they were not detected before or after the period of therapy with this immunosuppressive agent in any of the 6 cases. They interfered with crossmatch procedures for red cell transfusion, and were only variably removed by autoabsorption techniques. Heat treatment of sera containing MALG-related red cell antibodies was ineffective in abrogating their reactivity and also compromised the reactivity of some red cell alloantibodies which were tested as controls. Transfusion of ‘least-incompatible’ red blood cells had no adverse effects in 2 cases where it was necessitated by clinical circumstances, despite an inability to obtain suitable serological samples for crossmatching