Kidd blood group system: a review

Abstract

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.

A case of mistaken MELD (model for end stage liver disease) score—How an acute hemolytic transfusion reaction falsely altered a patient's transplant status

“…The patient had a steady increase in bilirubin which gradually increased the MELD score to 34. However, after experiencing the AHTR, his bilirubin increased from 4.7 to 17.1 mg/dl, which significantly increased his MELD score to his highest score of 41, which altered his predicted 3‐month survival to 30% 5 . The patient's MELD score started to improve (MELD score of 35) after resolution of the acute hemolysis with a subsequent decrease in bilirubin (Figure 2).…”

“…JK antibodies are notorious for causing delayed hemolytic transfusion reactions (DHTR) due to their tendency to drop to low or undetectable levels in the plasma and be missed in pre‐transfusion testing 3 . Notably, they can also cause AHTR due to their ability to activate complement, although the likelihood of complement fixation has been challenged in some studies 4,5 . Anti‐Jk also appear to be predominantly IgG1 and IgG3 subtypes, with a higher association with acute hemolysis than IgG2 and IgG4 5 .…”

“…Notably, they can also cause AHTR due to their ability to activate complement, although the likelihood of complement fixation has been challenged in some studies 4,5 . Anti‐Jk also appear to be predominantly IgG1 and IgG3 subtypes, with a higher association with acute hemolysis than IgG2 and IgG4 5 . AHTR is characterized clinically by fever, chills, hypotension, back pain, and disseminated intravascular hemolysis (DIC).…”

Kidd (SLC14A1 rs1058396) Genotyping Performed by PCR-Restriction Fragment Length Polymorphism Using a General-Purpose Agarose Gel and Lithium Borate Buffer

“…Kidd 혈액형군은 Jk a , Jk b 와 Jk3 항원으로 구성 되어 있으며, Kidd 혈액형은 임상적으로 용혈수 혈반응 및 태아신생아용혈성질환을 일으키는 빈도가 비교적 높은 혈액형이다 [1][2][3]. Kidd 혈액 형군의 유전정보는 SLC14A1 (Solute Carrier Family 14 Member 1)유전자에 있으며, SLC14A1 rs1058396 변이에 따라 JK*01과 JK*02로 유전형 이 결정된다 [1].…”

“…Kidd 혈액형군은 Jk a , Jk b 와 Jk3 항원으로 구성 되어 있으며, Kidd 혈액형은 임상적으로 용혈수 혈반응 및 태아신생아용혈성질환을 일으키는 빈도가 비교적 높은 혈액형이다 [1][2][3]. Kidd 혈액 형군의 유전정보는 SLC14A1 (Solute Carrier Family 14 Member 1)유전자에 있으며, SLC14A1 rs1058396 변이에 따라 JK*01과 JK*02로 유전형 이 결정된다 [1]. 이 단일염기변이를 검출하기 위해 PCR-RFLP (restriction fragment length polymorphism) [3,4], Allele-specific PCR [5,6], SNaPshot [7]과 real-time PCR [8] 등 다양한 기법이 소개되어 JK 유 전형을 판정하는데 이용되고 있다.…”