title: Possible suppression of fetal erythropoiesis by the Kell blood group antibody anti-Kp(a).
abstract: Antibodies to antigens in the Kell blood group system are usually immunoglobulin G, and, notoriously, anti-K, anti-k, and anti-Kp(a) can cause severe hemolytic transfusion reactions, as well as severe hemolytic disease of the fetus and newborn (HDFN). It has been shown that the titer of anti-K does not correlate with the severity of HDFN because, in addition to immune destruction of red blood cells (RBCs), anti-K causes suppression of erythropoiesis in the fetus, which can result in severe anemia. We report a case involving anti-Kp(a) in which one twin was anemic and the other was not. Standard hemagglutination and polymerase chain reaction (PCR)-based tests were used. At delivery, anti-Kp(a) was identified in serum from the mother and twin A, and in the eluate prepared from the baby’s RBCs. PCR-based assays showed twin A (boy) was KEL*841T/C (KEL*03/KEL*04), which is predicted to encode Kp(a+b+). Twin B (girl) was KEL*841C/C (KEL*04/KEL*04), which is predicted to encode Kp(a–b+). We describe the first reported case of probable suppression of erythropoiesis attributable to anti-Kp(a). One twin born to a woman whose serum contained anti-Kp(a) experienced HDFN while the other did not. Based on DNA analysis, the predicted blood type of the affected twin was Kp(a+b+) and that of the unaffected twin was Kp(a–b+). The laboratory findings and clinical course of the affected twin were consistent with suppression of erythropoiesis in addition to immune RBC destruction.
authors.affiliation: Trinity Health, Farmington Hills, MI, USA.
authors.forename: M
authors.initials: M
authors.lastname: Tuson
authors.forename: K
authors.initials: K
authors.lastname: Hue-Roye
authors.forename: K
authors.initials: K
authors.lastname: Koval
authors.forename: S
authors.initials: S
authors.lastname: Imlay
authors.forename: R
authors.initials: R
authors.lastname: Desai
authors.forename: G
authors.initials: G
authors.lastname: Garg
authors.forename: E
authors.initials: E
authors.lastname: Kazem
authors.forename: D
authors.initials: D
authors.lastname: Stockman
authors.forename: J
authors.initials: J
authors.lastname: Hamilton
authors.forename: M E
authors.initials: ME
authors.lastname: Reid
mesh_terms: D000328:Adult; D000906:Antibodies / Q000097:blood / Q000276:immunology*; D001787:Blood Group Incompatibility / Q000150:complications / Q000235:genetics* / Q000276:immunology / Q000503:physiopathology; D001788:Blood Grouping and Crossmatching; D003602:Cytotoxicity, Immunologic; D004899:Erythroblastosis, Fetal / Q000209:etiology / Q000235:genetics* / Q000276:immunology / Q000503:physiopathology; D004912:Erythrocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004920:Erythropoiesis / Q000235:genetics / Q000276:immunology; D005260:Female; D047109:Fetal Development; D005838:Genotype; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007626:Kell Blood-Group System / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D008297:Male; D010641:Phenotype; D014429:Twins, Dizygotic / Q000235:genetics
chemical_list: D000906:Antibodies; D007626:Kell Blood-Group System