Absence of hemolytic disease of fetus and newborn despite maternal high-titer IgG anti-Ku

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Immunohematology

American National Red Cross

Subject: Medical Laboratory Technology

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ISSN: 0894-203X
eISSN: 1930-3955

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VOLUME 26 , ISSUE 3 (September 2010) > List of articles

Absence of hemolytic disease of fetus and newborn despite maternal high-titer IgG anti-Ku

Ram M. Kakaiya / Angelica Whaley / Christine Howard-Menk / Jigna Rami / Mona Papari / Sally Campbell-Lee / Zbigniew Malecki

Keywords : Kell blood group, anti-Ku, Kell-null, K0, hemolytic disease of fetus and newborn, maternal alloimmunization, newborn hyperbilirubinemia, autologous blood donation, immunohematology

Citation Information : Immunohematology. Volume 26, Issue 3, Pages 119-122, DOI: https://doi.org/10.21307/immunohematology-2019-211

License : (Transfer of Copyright)

Published Online: 14-March-2020

ARTICLE

ABSTRACT

Anti-Ku seen in K0 (Kell-null) individuals has previously been shown to cause severe hemolytic transfusion reactions. Maternal anti-Ku can cause none or moderate to severe hemolytic disease of the fetus and newborn (HDFN). In two of four previously described HDFN cases, intrauterine transfusions were required because of severe anemia. We report a case in which maternal anti-Ku did not cause HDFN. Standard serologic methods were used for RBC antibody screening and identification, adsorption and elution of RBC antibodies, and antigen typing. A gravida 3, para 3 (G3P3) woman was first evaluated in 2006 and was found to have an IgG RBC antibody that reacted against all panel RBCs in the anti-human globulin phase. A panel of RBCs treated with DTT did not react with the antibody.  The antibody failed to react with one example of K0 RBCs. The patient’s RBCs typed negative for the following Kell blood group antigens: KEL1, KEL2, KEL3, KEL4, KEL6, KEL7, KEL11, KEL13, and KEL18. These results established the presence of anti-Ku in maternal serum. The newborn was group A, D+ and required phototherapy for hyperbilirubinemia, but did not require transfusion. The woman was seen again in January 2010 during the third trimester (G4P3). At this time, anti-Ku titer was 256. She delivered a healthy group O, D+ baby boy at 37 weeks’ gestation. Cord RBCs were 4+ for IgG by DAT. An eluate reacted with all RBCs tested, but did not react when tested against a panel of DTT-treated RBCs. K0 phenotype is rare to begin with, and the maternal anti-Ku formation may require more than one pregnancy. Therefore, cases that can be evaluated for anti-Ku–related HDFN are rare. Our case contributes to serologic and clinical aspects of such rare cases.

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