The Kidd blood group system has been recognized as clinically important in red blood cell (RBC) serology since its identification in 1951. Forty years later, the JK glycoprotein was determined to be a product of SCL14A1 and was identical to the urea transport protein UT-B produced by HUT11A. The functional role of the protein as a urea transporter in RBCs and kidney has been well documented. The polymorphism responsible for the antithetical antigens Jk a and Jk b was identified in 1994 as c.838G>A (p. Asp280Asn). Recent discoveries have expanded the system to include 23 variant alleles recognized by the International Society of Blood Transfusion that silence the protein expression and 7 variant alleles presumably producing weak or partial JK antigens. Null phenotypes have been identified in individuals of several populations including those of African, Indian, and Chinese decent, in addition to the well-documented findings in the Polynesian and Finnish populations. This review will examine the historical information about the antigens and antibodies of the JK system as well as catalog the variations of the JK gene.

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The basics of the Kidd blood group system have been well described. Two of the three antigens, Jka and Jkb, are polymorphic. The third, Jk3, is of very high prevalence in all populations except in individuals of Polynesian and Finnish extraction. Jk (a−b−) red cells do not express Jk3. The antigens are encoded by SLC14A1 gene on chromosome 18. JK*01 allele differs from JK*02 at nt 838 (G/A) and in the protein, at amino acid 280, Jka expression is associated with aspartate and asparagine is associated with Jkb. The genetic background of the dominantly inherited In(Jk) Jk(a−b−) is due to an 84 bp deletion in ZFN850 on chromosome 19. Antibodies against all three antigens are clinically important. They can cause immediate haemolytic transfusion reactions and are a frequent cause of delayed transfusion reactions. Haemolytic disease of the foetus and newborn due to JK antibodies is generally much less severe than the response to incompatible transfusion. The JK protein on red cells functions as a urea transporter. Complexity in the system is due to the number of alternate alleles described. ISBT recognizes 24 alleles that silence Jka/Jkb expression and 7 alleles causing weak or partial expression of Jka or Jkb. These alleles can result in serological typing discrepancies, discordant serological/molecular results and production of an apparent Kidd alloantibody by an antigen‐positive individual. JK antigens may serve as minor histocompatibility antigens. The antibodies may play a role in renal graft survival when a JK‐incompatible donor kidney is transplanted.

A saline–indirect antiglobulin test (IAT) is performed without addition of enhancement media to increase the binding of antibody to the red blood cell antigen during the 37°C incubation. Although infrequently used as a primary means for antibody detection or identification, this test is useful because of the variety of possible applications in antibody identification studies. It is critical to the test sensitivity to allow enough incubation time (30–60 minutes) for maximum antibody binding to occur. The saline test can also be subject to a direct agglutination reading after immediate spin, room temperature, or incubation at 37°C before conversion to the IAT. This step allows further flexibility in assessing the reactivity of directly agglutinating allo- or autoantibodies in tests performed at 37°C or lower temperatures.

http://onlinelibrary.wiley.com/doi/10.1111/trf.15709/full