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A screening program was implemented to identify hrB– donors. D– C+, D–C–, and D+C– samples from African-American donors were typed with multiple examples of anti-hrB and anti-hrB-like, and one example each of anti-V and anti-VS. Of 75 D–C+ donors, 4 (5%) typed as hrB–, and 14 others had weak or variable expression of hrB. Of these 18 individuals, 15 were V–VS+, and 3 were V+VS+. No hrB– sample was found in 90 C– donors, 26 of whom were V+VS+, and 1 was V–VS+. A review of our records of 44 hrB– patients and donors studied earlier revealed that at least 12, and possibly as many as 30, carried r′ or r′s . All hrB– donors found in our screening program had D–C+VS+ RBCs, indicating an overrepresentation of r′. Our record review also showed that the presence of r′ and r′s more often results in hrB– RBCs, and that the most effective way to screen for hrB– donors is to type African Americans who have D–C+ RBCs. Immunohematology 1995;11:74–77.

The red cells of a white male blood donor typed as Rh:–1, –2, –3,w4,w5,6,–17,w19,–31,–32,–34, and –46. Although the donor has no history of transfusion, his serum contains an alloantibody that is weakly reactive with most red blood cells (RBCs) tested. Only Rhnull and D–– RBCs are nonreactive. Reactivity is enhanced with ficin- or papain-treated RBCs and is unaffected by AET or DTT treatment of the RBCs. Previously described Rh:–46 RBCs have been of deletion types D––, D••, and Rhnull or Rh:32. In three multitransfused patients, the Rh46 antigen was temporarily suppressed and the phenotype eventually reverted to normal. This is the first report of RBCs of the Rh:–32,–46 phenotype that are not of a rare Rh deletion or Rhnull type. In addition, the Rh:w5,w19,–31,–34 phenotype is rarely found in whites. Immunohematology 1994; 10:130–133.