Lawicki Shaun, Covin Randal B, Powers Amy A
John A. Burns School of Medicine University of Hawai'i at Mānoa UH Pathology Residency Program Office, Honolulu, HI; Queens Medical Center, Honolulu, HI.
Blood Bank of Hawaii, Honolulu, HI.
Transfus Med Rev. 2017 Jul;31(3):165-172. doi: 10.1016/j.tmrv.2016.10.003. Epub 2016 Nov 9.
The Kidd blood group system was discovered in 1951 and is composed of 2 antithetical antigens, Jk and Jk, along with a third high-incidence antigen, Jk3. The Jk3 antigen is expressed in all individuals except those with the rare Kidd-null phenotype. Four Kidd phenotypes are therefore possible: Jk(a+b-), Jk(a-b+), Jk(a+b+), and Jk(a-b-). The glycoprotein carrying the Kidd antigens is a 43-kDa, 389-amino acid protein with 10 membrane-spanning domains which functions as a urea transporter on endothelial cells of the renal vasa recta as well as erythrocytes. The HUT11/UT-B/JK (SLC14A1) gene encoding this glycoprotein is located on chromosome 18q12-q21. The Jk and Jk antigens are the result of a single-nucleotide polymorphism present at nucleotide 838 resulting in an aspartate or asparagine amino acid at position 280, respectively. The Kidd blood group can create several difficult transfusion situations. Besides the typical acute hemolytic transfusion reactions common to all clinically relevant blood group antigens, the Kidd antigens are notorious for causing delayed hemolytic transfusion reactions due to the strong anamnestic response exhibited by antibodies directed against Kidd antigens. The Kidd-null phenotype is extremely rare in most ethnic groups, but is clinically significant due to the ability of those with the Kidd-null phenotype to produce antibodies directed against the high-incidence Jk3 antigen. Anti-Jk3 antibodies behave in concordance with anti-Jk or anti-Jk possessing the capability to cause both acute and delayed hemolytic reactions. Antibodies against any of the 3 Kidd antigens can also be a cause of hemolytic disease of the fetus and newborn, although this is generally mild. In this review, we will outline the makeup of the Kidd system from its historical discovery to the details of the Kidd gene and glycoprotein, and then discuss the practical aspects of Kidd antibodies and transfusion reactions with an extended focus on the Kidd-null phenotype. We will end with a brief discussion of the donor aspects related to the screening and supply management of blood from donors with the rare Jk(a-b-) phenotype.
基德血型系统于1951年被发现，由两种对立抗原Jk(a)和Jk(b)以及第三种高频率抗原Jk3组成。除了具有罕见的基德无效表型的个体外，Jk3抗原在所有个体中均有表达。因此，可能存在四种基德表型：Jk(a+b-)、Jk(a-b+)、Jk(a+b+)和Jk(a-b-)。携带基德抗原的糖蛋白是一种43 kDa、含389个氨基酸的蛋白质，具有10个跨膜结构域，在直小血管内皮细胞和红细胞中作为尿素转运体发挥作用。编码这种糖蛋白的HUT11/UT-B/JK(SLC14A1)基因位于18号染色体q12-q21区域。Jk(a)和Jk(b)抗原是由第838位核苷酸处的单核苷酸多态性导致的，分别在第280位氨基酸处产生天冬氨酸或天冬酰胺。基德血型可能会引发多种输血难题。除了所有临床相关血型抗原常见的典型急性溶血性输血反应外，基德抗原还因针对基德抗原的抗体表现出强烈的回忆反应而导致迟发性溶血性输血反应而声名狼藉。基德无效表型在大多数种族中极为罕见，但由于具有基德无效表型的个体能够产生针对高频率Jk3抗原的抗体，因此具有临床意义。抗Jk3抗体的行为与抗Jk(a)或抗Jk(b)抗体一致，能够引发急性和迟发性溶血反应。针对三种基德抗原中任何一种的抗体也可能是胎儿和新生儿溶血病的病因，不过通常病情较轻。在本综述中，我们将概述基德系统的构成，从其历史发现到基德基因和糖蛋白的细节，然后讨论基德抗体和输血反应的实际问题，并特别关注基德无效表型。最后，我们将简要讨论与罕见Jk(a-b-)表型献血者的筛查和血液供应管理相关的献血者方面的问题。
