Tools
Kidd Blood Group System
Introduction
The Kidd blood group system is a collection of 3 glycoprotein antigens on the surface of red blood cells (RBCs) and the vasa recta of the kidneys. These antigens are absent on other cell surfaces and tissues. The glycoprotein has the physiological function of transporting urea across membranes.[1][2] In 1951, Allen et al discovered the Kidd blood group system in a pregnant woman whose baby died of erythroblastosis fetalis. This unknown antibody was termed anti-Jka in the memory of John Kidd. Two other antigens, Jkb and Jk3, were also discovered later on. The Kidd null phenotype Jk(a−b−) was found in 1959 in a Filipino woman who developed jaundice with a blood transfusion.[3] The antigens of the Kidd blood group system are multipass transmembrane proteins, and they span the RBC membrane 10 times. These antigens are characterized by having their amino (−NH2) terminal and carboxyl (−COOH) terminal located intracytoplasmic.[4] In 1994, B Olives et al isolated a complementary DNA HUT11 from human bone marrow encoding a urea transporter, which was 80% similar to urea transporter UT3 in rats.[5]
The solute carrier family 14 member 1 (SLC14A1) gene is located on the long arm of chromosome 18 (18q12.3), which encodes for the Kidd blood group antigens in human erythrocytes. The SLC14A1 gene symbolized as HUT11 or JK encodes a membrane glycoprotein that functions as a urea transporter expressed on the erythrocytes. This gene has 28,340 nucleotide base pairs and 13 exons encoding the mature protein for Kidd antigen. The Jka and Jkb antigens differ by a single amino acid due to a single nucleotide polymorphism on the fourth extracellular loop of the Kidd glycoprotein at change sequence of single amino acid variation as Asp280 (aspartic acid in Jka) and Asn280 (asparagine in Jkb). This transition mutation replaces an adenine (A) with a guanine (G) nucleotide, resulting in the Asp280Asn substitution.[6]
International Society of Blood Transfusion (ISBT) symbol for Kidd blood group system: JK
International Society of Blood Transfusion (ISBT) number for Kidd blood group system: 009
The Kidd blood group system consists of three antigens present on RBCs—Jka, Jkb, and Jk3. These antigens are not found on granulocytes, lymphocytes, monocytes, and platelets. Similar to other Kidd antigens, Kidd antigens are resistant to ficin, papain, trypsin, chymotrypsin, and pronase. Furthermore, the reactivity of Kidd antibodies is enhanced by these proteolytic enzymes during testing.[7][8][9]
- ISBT symbol: Jk1
- ISBT number: 009.001
- Antithetical antigen: Jkb (Jk2)
- Cord blood RBCs: Expressed on the fetal RBCs as early as 11 weeks of gestation.
- ISBT symbol: Jk2
- ISBT number: 009.002
- Antithetical antigen: Jka (Jk1)
- Cord blood RBCs: Expressed on the fetal RBCs as early as 11 weeks of gestation.
- ISBT symbol: Jk3
- ISBT number: 009.003
- High-prevalence antigen, with a frequency of nearly 100% in all populations (>99% in Polynesians)
- Cord blood RBCs: Jk3 is expressed on erythroblasts at a late stage of erythropoiesis
The major Kidd phenotypes are Jk(a+b−), Jk(a−b+), Jk(a+b+), and Jk(a−b−). The Jk(a−b−) phenotype or Kidd null phenotype is rare and lacks all Jka, Jkb, and Jk3 antigens. As Jk3 is a high-prevalence antigen, individuals who developed anti-Jk3 antibodies require blood transfusions from donors with the rare null phenotype. Kidd null phenotype is most abundant among Polynesians. A screening method for identifying individuals with the Kidd null phenotype involves delayed lysis of their RBCs in a 2M urea solution. These individuals show no clinical abnormality, but their capability of concentrating urine is reduced by one-third.[10][11]
Table. Major antigenic frequencies of the Kidd phenotypes
|
Kidd Phenotype |
Whites |
Blacks |
Asians |
|
Jk(a+b−) |
26.3% |
51.1% |
23.2% |
|
Jk(a+b+) |
23.4% |
8.1% |
26.8% |
|
Jk(a−b+) |
50.3% |
40.8% |
49.1% |
|
Jk(a−b−) |
Rare |
Rare |
0.9% (Polynesians) |
Table reference: [12]
Antibodies against Kidd antigens can lead to acute and delayed hemolytic transfusion reactions. These antibodies are often involved in delayed hemolytic transfusion reactions as their level becomes undetectable with time and then rapidly increases upon re-exposure to Kidd antigens. The incidence of clinically significant red cell hemolysis due to Kidd antibodies is relatively rare but notable. These antibodies can trigger the complement system and can lead to intravascular hemolysis. The incidence of delayed hemolytic transfusion reactions is estimated from 1 in 1000 to 1 in 10,000 transfusion episodes.[13]
Kidd blood group antigens can be determined using various methodologies, broadly categorized into serological and molecular techniques. The urea hemolysis test is a traditional method that assesses the ability of RBCs to withstand osmotic stress in urea. The presence of Kidd antigens allows RBCs to lyse in urea, whereas those lacking these antigens remain intact. Although this test is straightforward, it may not always provide conclusive results for all phenotypes, particularly in partial or weak expression cases.[14] Direct and indirect antiglobulin tests are also used to detect specific antibodies against Kidd antigens in serum or plasma. The direct test checks for antibodies bound to the RBCs, whereas the indirect test assesses free antibodies in the serum. These methods are essential for confirming the presence of anti-Jk antibodies, especially in patients with a history of transfusions, as they help identify any unexpected antibodies that could lead to transfusion reactions.[15]
Polymerase chain reaction (PCR) is a highly sensitive molecular technique used to amplify specific DNA sequences associated with Kidd antigens. This method can identify genotypes corresponding to various Kidd phenotypes, making it particularly useful when serological methods yield inconclusive results. In addition, PCR can help predict the likelihood of hemolytic disease in the newborn (HDN) by determining maternal antibody status.[16] PCR-SSP (sequence-specific primers) employs primers that specifically bind to known sequences within the Kidd gene, allowing for accurate determination of Kidd phenotypes. This method is cost-effective and suitable for routine testing, especially in blood banks.[17][18] PCR-RFLP (restriction fragment length polymorphism) uses restriction enzymes to cut DNA at specific sites, enabling analysis of variations in the Kidd gene. This technique provides detailed information about genetic polymorphisms associated with different Kidd phenotypes.[19]
Microarray technology enables simultaneous analysis of multiple blood group antigens, including those in the Kidd system. This high-throughput method is efficient for large-scale screenings and can help identify rare phenotypes that might not be detectable through traditional serological methods.[20] Sanger sequencing can be used to analyze exons and intron-exon borders of the Kidd gene, providing comprehensive information about mutations and polymorphisms. This method is particularly valuable for identifying novel variants and understanding their clinical implications.[21]
Accurate determination of Kidd blood group antigens is crucial in transfusion medicine due to their association with delayed hemolytic transfusion reactions and hemolytic disease of the newborn. Although serological methods are quick and useful for initial assessments, molecular techniques offer higher sensitivity and specificity, especially in complex clinical scenarios, such as recent transfusions or autoimmune conditions. The choice of method often depends on available resources, clinical requirements, and the need for accuracy in transfusion matching.[18]
Function
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Function
Functions of Kidd Glycoprotein Antigen
In 1982, Heaton and McLoughlin established that the Kidd blood group system functions as a urea transporter across the RBC membrane. They discovered that RBCs of a Jk(a−b−) individual resist lysis in a 2M urea solution for 30 min, leading to falsely high platelet counts on testing with an automated cell counter. Red cells with common Kidd phenotypes are lysed within 1 min in 2M urea.[22] The RBCs of Kidd null individuals transport urea approximately 1000 times slower compared to normal individuals.[23] Gargus and Mitas proposed that the cosegregation of the absent Kidd antigen and urea transporter may suggest that these 2 proteins are identical. In 1994, the human urea transporter HUT11 was identified and later confirmed to be the protein carrying the Kidd blood group antigen.[5]
Two urea transporters, UT-A and UT-B, have been discovered in human kidneys. UT-B is the name given to the Kidd protein on the renal vasa recta and RBC membrane. UT-A, though it resembles UT-B, is only present in kidney cells.[18] Rapid urea transport occurs in RBCs when they enter or leave the renal medulla. The medulla has the highest urea concentration and is fundamental in concentrating urine. Without this transporter, the RBCs may be exposed to high osmotic differences, causing hypertonic lysis or hypotonic swelling. This function also helps maintain urea osmolarity in the renal medulla as the red cells transport urea out while leaving the medulla into the circulation.[24] The absence of this protein in Kidd null individuals hampers the kidneys' ability to concentrate urine maximally. However, there is no disease or change in the lifespan of RBCs.[11]
The pharmacological properties of the human red blood cell urea transporter (HUT11) and the kidney urea transporter (HUT2) have been compared. Both HUT11 and HUT2 facilitate the rapid transfer of urea without accompanying water. These transporters are inhibited by phloretin, but at different half-maximal inhibitory concentrations (IC50); HUT11 has an IC50 of 75 µM, whereas HUT2 has an IC50 of 230 µM. Notably, para-chloromercuribenzene sulfonate inhibits HUT11 at an IC50 of 150 µM but does not inhibit HUT2 at any tested concentration. Thus, while HUT11 and HUT2 facilitate rapid urea movement across cell membranes, they exhibit distinct pharmacological differences.[25]
Kidd Antibodies
Kidd antibodies are mostly IgG type with rare instances of IgM type. These antibodies can bind to complement and can lead to intravascular hemolysis. Kidd antibodies are typically formed in response to transfusion or pregnancy. Alloanti-Jka antibodies are more common compared to Alloanti-Jkb antibodies. Kidd antibodies are detected most commonly within a month of transfusion, but their levels decline rapidly and sometimes become undetectable after 3 months. These antibodies can show a strong anamnestic response when re-sensitized. Although most Kidd antibodies are alloantibodies formed due to pregnancy, transfusion, or transplantation, they may also occasionally be naturally occurring.[26][27]
Anti-Jka antibody production is associated with the HLA-DRB1*01 genotype. An antiglobulin test is required to detect Kidd antibodies in most cases. Sometimes, enzyme-treated red cells are needed to detect weaker antibodies. Most Anti-Jka antibodies react more strongly with Jk(a+b−) cells compared to Jk(a+b+) cells. Similarly, anti-Jkb antibodies react more strongly with Jk(a−b+) cells compared to Jk(a+b+) cells, demonstrating dosage phenomena in Kidd blood group system antibodies. Therefore, antibody identification panels should include both Jk(a+b) and Jk(a−b+) red cells. Kidd antibodies are often challenging to detect due to the evanescence effect. Some antibodies can agglutinate antigen-positive cells, but the reactions are typically weak. Sometimes, these antibodies may be missed if not tested in semiautomated or fully automated antibody identification platforms compared to the standard tube technique. Approximately 40% to 50% of sera with Kidd antibodies bind complement; these antibodies are sometimes only detectable in the antiglobulin test using polyspecific antiglobulin or anti-complement. Techniques that use diluent binding calcium may fail to detect some Kidd antibodies. Antibodies to the Kidd system may cause both acute and delayed hemolytic transfusion reactions, but most reported reactions are delayed types. These antibodies can also cause mild hemolytic disease in fetuses and newborns.[28][29]
Clinical Significance
Kidd Antibodies and Transfusion Reactions
Kidd antibodies, primarily of the IgG type, are clinically significant and may be weak, exhibiting dosage effects. Identifying such antibodies may require enzyme treatment and awareness of transfusion services. Kidd antibodies are implicated in both acute and delayed hemolytic transfusion reactions.[30] A significant reason for delayed HTRs is the rapid decline in antibody titer low or undetectable levels in the plasma after initial contact, leading to a severe anamnestic reaction in case of re-sensitization. Anti-Jka is involved in over one-third of delayed hemolytic transfusion reactions (HTRs).[31] Anti-Jka antibodies are responsible for mild-to-severe immediate HTRs and are regularly associated with delayed HTRs, which may lead to oliguria, renal failure, and even death. Anti-Jkb is also implicated in causing severe acute and delayed reactions. Anti-Jk3 may be formed if Kidd null patients are transfused with either of Jk(a+b−), Jk(a−b+), or Jk(a+b+) phenotypes. Anti-Jk3 has been proven to cause mild-to-severe HTRs. In such cases, a registry of Kidd null blood donors is paramount. The rarity of this phenotype in nearly all global populations makes it extremely difficult to transfuse such patients. Identifying such donors, cryopreservation, and formulating rare donor programs may play an essential role.[32]
Hemolytic Disease of the Fetus and Newborn
Kidd antigens may be responsible for causing alloimmunization in pregnant females, but the hemolytic disease of the fetus and newborn is typically mild, even with the presence of a very high titer, and only a few cases are reported.[33][34]
Passenger Lymphocyte Syndrome
A few cases of passenger lymphocyte syndrome are caused by anti-Jka antibodies following peripheral blood progenitor cell and liver transplantation in the follow-up phase, where they can be mild to severe and can lead to hemolysis.[35][36]
Kidd Antibodies and Renal Transplant
Kidd antibodies have been shown to cause aggressive acute and hyperacute kidney transplant rejections, possibly due to the structural similarity between urea transporters and Kidd antigens.[14] Anti-Jka and anti-Jkb cross-react with urea transporters in the transplanted kidney, potentially leading to rejection. This finding highlights the role of Kidd antigens as minor histocompatibility antigens in renal transplantation. In recent studies, it is evident that whenever there is a mismatch between donor and patient Kidd antigens, higher chances for interstitial inflammation are found in the Kidd unmatched recipients.[37][38]
SLC14A1 Gene and Bladder Cancer
Overexpression of the urea transporter gene SLC14A1 in cancer-associated fibroblasts is associated with unfavorable clinical outcomes in patients with bladder cancer. This gene may serve as a potential target for interferon activity. An inhibition of SLC14A1-positive cancer-associated fibroblast formation through STAT1 or STING pathway targeting can sensitize the bladder cancer cells to chemotherapy.[39]
Effect on Total Cholesterol Levels
Some studies suggest that individuals homozygous for Jka have higher total cholesterol levels compared to others, and the Jkb gene may have a restrictive effect on the variability of total cholesterol levels. Although there was no effect on high-density lipoprotein cholesterol or triglycerides, the reason has been postulated to be the variability gene.[40]
Enhancing Healthcare Team Outcomes
Prevention of transfusion reactions due to the Kidd blood group system requires a unified and interprofessional medical team to enhance patient safety and transfusion outcomes. Every healthcare staff in the transfusion chain plays a critical role in patient safety. The healthcare staff must check for an additional Kidd antigen-negative blood unit with all mandatory pretransfusion checks during the planning of transfusion in patients with Kidd antibodies.
All healthcare staff should know their responsibilities in the transfusion team. During transfusing blood products, nurses and clinicians should be proficient in promptly identifying transfusion reactions and possible complications while implementing close monitoring and preventive strategies to handle adversities. Obtaining informed consent from patients regarding anti-Kidd antibodies is crucial for respecting their autonomy and ensuring beneficence and non-maleficence. In managing adverse transfusion events caused by kidd antibodies, an interprofessional healthcare team can ensure better responsiveness, minimize complications, and prioritize patient safety. Further research should be conducted on the role of the SLC14A1 gene and its functional protein in various diseases, along with the transfusion outcomes and its clinical sequelae.
References
Cartron JP, Ripoche P. Urea transport and Kidd blood groups. Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine. 1995:2(4):309-15 [PubMed PMID: 8542029]
Sidoux-Walter F, Lucien N, Olivès B, Gobin R, Rousselet G, Kamsteeg EJ, Ripoche P, Deen PM, Cartron JP, Bailly P. At physiological expression levels the Kidd blood group/urea transporter protein is not a water channel. The Journal of biological chemistry. 1999 Oct 15:274(42):30228-35 [PubMed PMID: 10514515]
PLAUT G, IKIN EW, MOURANT AE, SANGER R, RACE RR. A new blood-group antibody, anti Jkb. Nature. 1953 Mar 7:171(4349):431 [PubMed PMID: 13046499]
Hamilton JR. Kidd blood group system: a review. Immunohematology. 2015:31(1):29-35 [PubMed PMID: 26308468]
Olives B, Neau P, Bailly P, Hediger MA, Rousselet G, Cartron JP, Ripoche P. Cloning and functional expression of a urea transporter from human bone marrow cells. The Journal of biological chemistry. 1994 Dec 16:269(50):31649-52 [PubMed PMID: 7989337]
Shi J, Sha R, Yang X. Role of the human solute carrier family 14 member 1 gene in hypoxia-induced renal cell carcinoma occurrence and its enlightenment to cancer nursing. BMC molecular and cell biology. 2023 Mar 18:24(1):10. doi: 10.1186/s12860-023-00473-6. Epub 2023 Mar 18 [PubMed PMID: 36934247]
Lawicki S, Covin RB, Powers AA. The Kidd (JK) Blood Group System. Transfusion medicine reviews. 2017 Jul:31(3):165-172. doi: 10.1016/j.tmrv.2016.10.003. Epub 2016 Nov 9 [PubMed PMID: 28065763]
Bony V, Gane P, Bailly P, Cartron JP. Time-course expression of polypeptides carrying blood group antigens during human erythroid differentiation. British journal of haematology. 1999 Nov:107(2):263-74 [PubMed PMID: 10583211]
Dunstan RA. Status of major red cell blood group antigens on neutrophils, lymphocytes and monocytes. British journal of haematology. 1986 Feb:62(2):301-9 [PubMed PMID: 3511947]
Henry S, Woodfield G. Frequencies of the Jk(a-b-) phenotype in Polynesian ethnic groups. Transfusion. 1995 Mar:35(3):277 [PubMed PMID: 7878726]
Sands JM, Gargus JJ, Fröhlich O, Gunn RB, Kokko JP. Urinary concentrating ability in patients with Jk(a-b-) blood type who lack carrier-mediated urea transport. Journal of the American Society of Nephrology : JASN. 1992 Jun:2(12):1689-96 [PubMed PMID: 1498276]
Makroo RN, Bhatia A, Gupta R, Phillip J. Prevalence of Rh, Duffy, Kell, Kidd & MNSs blood group antigens in the Indian blood donor population. The Indian journal of medical research. 2013 Mar:137(3):521-6 [PubMed PMID: 23640559]
Tormey CA, Hendrickson JE. Transfusion-related red blood cell alloantibodies: induction and consequences. Blood. 2019 Apr 25:133(17):1821-1830. doi: 10.1182/blood-2018-08-833962. Epub 2019 Feb 26 [PubMed PMID: 30808636]
Barros MMO. Kidd system antigens and kidney disease. Revista brasileira de hematologia e hemoterapia. 2017 Oct-Dec:39(4):293-294. doi: 10.1016/j.bjhh.2017.07.004. Epub 2017 Oct 12 [PubMed PMID: 29150097]
Theis SR, Hashmi MF. Coombs Test. StatPearls. 2025 Jan:(): [PubMed PMID: 31613487]
Intharanut K, Grams R, Bejrachandra S, Sriwanitchrak P, Nathalang O. Improved allele-specific PCR technique for Kidd blood group genotyping. Journal of clinical laboratory analysis. 2013 Jan:27(1):53-8. doi: 10.1002/jcla.21561. Epub [PubMed PMID: 23325744]
Prager M. Molecular genetic blood group typing by the use of PCR-SSP technique. Transfusion. 2007 Jul:47(1 Suppl):54S-9S [PubMed PMID: 17593287]
Quirino MG, Colli CM, Macedo LC, Sell AM, Visentainer JEL. Methods for blood group antigens detection: cost-effectiveness analysis of phenotyping and genotyping. Hematology, transfusion and cell therapy. 2019 Jan-Mar:41(1):44-49. doi: 10.1016/j.htct.2018.06.006. Epub 2018 Oct 30 [PubMed PMID: 30793104]
Jalali SF, Oodi A, Azarkeivan A, Gudarzi S, Amirizadeh N. Kidd Blood Group Genotyping for Thalassemia Patient in Iran. Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion. 2020 Jul:36(3):550-555. doi: 10.1007/s12288-020-01283-y. Epub 2020 Apr 29 [PubMed PMID: 32647431]
Boccoz SA, Le Goff G, Blum LJ, Marquette CA. Microarrays in blood group genotyping. Methods in molecular biology (Clifton, N.J.). 2015:1310():105-13. doi: 10.1007/978-1-4939-2690-9_9. Epub [PubMed PMID: 26024629]
Liang S, Su YQ, Liang YL, Wu F, Zhang H, Shi JH, Hong WX, Xu YP. DNA sequence analysis and Jk blood group genotype-phenotype assessment. Annals of translational medicine. 2020 Oct:8(19):1242. doi: 10.21037/atm-20-6504. Epub [PubMed PMID: 33178774]
Tsukaguchi H, Shayakul C, Berger UV, Tokui T, Brown D, Hediger MA. Cloning and characterization of the urea transporter UT3: localization in rat kidney and testis. The Journal of clinical investigation. 1997 Apr 1:99(7):1506-15 [PubMed PMID: 9119994]
Heaton DC, McLoughlin K. Jk(a-b-) red blood cells resist urea lysis. Transfusion. 1982 Jan-Feb:22(1):70-1 [PubMed PMID: 7064211]
Macey RI, Yousef LW. Osmotic stability of red cells in renal circulation requires rapid urea transport. The American journal of physiology. 1988 May:254(5 Pt 1):C669-74 [PubMed PMID: 3364552]
Martial S, Olivès B, Abrami L, Couriaud C, Bailly P, You G, Hediger MA, Cartron JP, Ripoche P, Rousselet G. Functional differentiation of the human red blood cell and kidney urea transporters. The American journal of physiology. 1996 Dec:271(6 Pt 2):F1264-8 [PubMed PMID: 8997401]
Schonewille H, van de Watering LM, Loomans DS, Brand A. Red blood cell alloantibodies after transfusion: factors influencing incidence and specificity. Transfusion. 2006 Feb:46(2):250-6 [PubMed PMID: 16441603]
Kim HH, Park TS, Lee W, Lee SD, Kim HO. Naturally occurring anti-Jk(a). Transfusion. 2005 Jun:45(6):1043-4 [PubMed PMID: 15935011]
Schonewille H, van de Watering LM, Brand A. Additional red blood cell alloantibodies after blood transfusions in a nonhematologic alloimmunized patient cohort: is it time to take precautionary measures? Transfusion. 2006 Apr:46(4):630-5 [PubMed PMID: 16584440]
Deb J, Kaur D, Sil S, Bava D, Mohan KA, Jain A, Negi G. Delayed haemolytic transfusion reaction due to Kidd antibodies. Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine. 2022 Aug:29(3):269-272. doi: 10.1016/j.tracli.2022.03.001. Epub 2022 Mar 11 [PubMed PMID: 35288280]
Pineda AA, Taswell HF, Brzica SM Jr. Transfusion reaction. An immunologic hazard of blood transfusion. Transfusion. 1978 Jan-Feb:18(1):1-7 [PubMed PMID: 415392]
Pineda AA, Vamvakas EC, Gorden LD, Winters JL, Moore SB. Trends in the incidence of delayed hemolytic and delayed serologic transfusion reactions. Transfusion. 1999 Oct:39(10):1097-103 [PubMed PMID: 10532604]
Velasco Rodríguez D, Pérez-Segura G, Jiménez-Ubieto A, Rodríguez MA, Montejano L. Hemolytic disease of the newborn due to anti-jkb: case report and review of the literature. Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion. 2014 Jun:30(2):135-8. doi: 10.1007/s12288-012-0202-7. Epub 2012 Oct 9 [PubMed PMID: 24839369]
Level 3 (low-level) evidenceMittal K, Sood T, Bansal N, Bedi RK, Kaur P, Kaur G. Clinical Significance of Rare Maternal Anti Jk(a) Antibody. Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion. 2016 Dec:32(4):497-499 [PubMed PMID: 27812263]
Lawicki S, Coberly EA, Lee LA, Johnson M, Eichbaum Q. Jk3 alloantibodies during pregnancy-blood bank management and hemolytic disease of the fetus and newborn risk. Transfusion. 2018 May:58(5):1157-1162. doi: 10.1111/trf.14548. Epub 2018 Feb 25 [PubMed PMID: 29479723]
Migdady Y, Pang Y, Kalsi SS, Childs R, Arai S. Post-hematopoietic stem cell transplantation immune-mediated anemia: a literature review and novel therapeutics. Blood advances. 2022 Apr 26:6(8):2707-2721. doi: 10.1182/bloodadvances.2021006279. Epub [PubMed PMID: 34972204]
Level 3 (low-level) evidenceHareuveni M, Merchav H, Austerlitz N, Rahimi-Levene N, Ben-Tal O. Donor anti-Jk(a) causing hemolysis in a liver transplant recipient. Transfusion. 2002 Mar:42(3):363-7 [PubMed PMID: 11961243]
Holt S, Donaldson H, Hazlehurst G, Varghese Z, Contreras M, Kingdon E, Sweny P, Burns A. Acute transplant rejection induced by blood transfusion reaction to the Kidd blood group system. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 2004 Sep:19(9):2403-6 [PubMed PMID: 15299103]
Holt SG, Kotagiri P, Hogan C, Hughes P, Masterson R. The potential role of antibodies against minor blood group antigens in renal transplantation. Transplant international : official journal of the European Society for Organ Transplantation. 2020 Aug:33(8):841-848. doi: 10.1111/tri.13685. Epub [PubMed PMID: 32619297]
Ma Z, Li X, Mao Y, Wei C, Huang Z, Li G, Yin J, Liang X, Liu Z. Interferon-dependent SLC14A1(+) cancer-associated fibroblasts promote cancer stemness via WNT5A in bladder cancer. Cancer cell. 2022 Dec 12:40(12):1550-1565.e7. doi: 10.1016/j.ccell.2022.11.005. Epub 2022 Dec 1 [PubMed PMID: 36459995]
Berg K. Variability gene effect on cholesterol at the Kidd blood group locus. Clinical genetics. 1988 Feb:33(2):102-7 [PubMed PMID: 3359662]