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基德血型系统与慢性肾脏病之间无关联。

Lack of association between Kidd blood group system and chronic kidney disease.

作者信息

Capriolli Tiago Verri, Visentainer Jeane Eliete Laguila, Sell Ana Maria

机构信息

Universidade Estadual de Maringá (UEM), Maringá, PR, Brazil.

Universidade Estadual de Maringá (UEM), Maringá, PR, Brazil.

出版信息

Rev Bras Hematol Hemoter. 2017 Oct-Dec;39(4):301-305. doi: 10.1016/j.bjhh.2017.05.007. Epub 2017 Jun 28.

DOI:10.1016/j.bjhh.2017.05.007
PMID:29150101
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5693269/
Abstract

BACKGROUND

The Kidd blood group system has three antigens, Jk, Jk and Jk3, found on red blood cells and on endothelial cells of the inner lining of blood vessels in the renal medulla. These are known as urea transporter B (UT-B). Researchers have found that individuals carrying the Jk(a-b-) or Jk-null (UT-B null) phenotypes have a lower urine-concentrating capability and risk of severe renal impairment. This study evaluated the distribution of the Kidd phenotypes in patients with chronic kidney disease and a possible association of Kidd antigens with the development of renal disease.

METHODS

Jk and Jk antigens were phenotyped using the gel column agglutination test (ID-cards Bio-RAD) in 197 patients with chronic kidney disease and 444 blood donors, as the control group. The phenotype and antigen frequencies between patients and controls were evaluated using the Chi-square method with Yates correction and logistic regression after adjustments for gender and age.

RESULTS

No differences were observed between the Kidd phenotypes frequency distribution between patients with chronic kidney disease and blood donors [Jk(a-b+)=22.3% and 27.2%; Jk(a+b-)=30.5% and 24.3%; Jk(a+b+)=47.25% and 48.4%, respectively].

CONCLUSION

The distribution of Kidd phenotypes found in the studied population is expected for Caucasians; Jk and Jk antigens and phenotypes were not found to be related to susceptibility for chronic kidney disease.

摘要

背景

基德血型系统有三种抗原,即Jk、Jk和Jk3,存在于红细胞以及肾髓质血管内衬的内皮细胞上。这些抗原被称为尿素转运蛋白B(UT-B)。研究人员发现,携带Jk(a-b-)或Jk缺失(UT-B缺失)表型的个体尿液浓缩能力较低,且有严重肾功能损害的风险。本研究评估了慢性肾脏病患者中基德表型的分布情况以及基德抗原与肾脏疾病发生之间可能存在的关联。

方法

采用凝胶柱凝集试验(ID卡,伯乐公司)对197例慢性肾脏病患者和444名献血者(作为对照组)进行Jk和Jk抗原表型分析。采用校正Yates的卡方检验以及在对性别和年龄进行校正后的逻辑回归分析,评估患者与对照组之间的表型和抗原频率。

结果

慢性肾脏病患者与献血者的基德表型频率分布未观察到差异[Jk(a-b+)=22.3%和27.2%;Jk(a+b-)=30.5%和24.3%;Jk(a+b+)=47.25%和48.4%,分别]。

结论

在研究人群中发现的基德表型分布符合白种人的预期情况;未发现Jk和Jk抗原及表型与慢性肾脏病易感性相关。

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本文引用的文献

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Erythrogene: a database for in-depth analysis of the extensive variation in 36 blood group systems in the 1000 Genomes Project.红细胞基因数据库:用于深入分析千人基因组计划中36个血型系统的广泛变异。
Blood Adv. 2016 Dec 16;1(3):240-249. doi: 10.1182/bloodadvances.2016001867. eCollection 2016 Dec 27.
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The evolving science of apolipoprotein-L1 and kidney disease.载脂蛋白L1与肾脏疾病的科学进展
Curr Opin Nephrol Hypertens. 2016 May;25(3):217-25. doi: 10.1097/MNH.0000000000000222.
3
Developmental Origins for Kidney Disease Due to Shroom3 Deficiency.Shroom3 缺乏导致的肾脏疾病的发育起源
J Am Soc Nephrol. 2016 Oct;27(10):2965-2973. doi: 10.1681/ASN.2015060621. Epub 2016 Mar 3.
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Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.53个基因座的遗传关联揭示了与肾功能相关的细胞类型和生物学途径。
Nat Commun. 2016 Jan 21;7:10023. doi: 10.1038/ncomms10023.
5
Kidd blood group system: a review.基德血型系统综述
Immunohematology. 2015;31(1):29-35.
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Clinical aspects of urea transporters.尿素转运蛋白的临床方面。
Subcell Biochem. 2014;73:179-91. doi: 10.1007/978-94-017-9343-8_12.
7
Chapter 1: Definition and classification of CKD.第1章:慢性肾脏病的定义和分类。
Kidney Int Suppl (2011). 2013 Jan;3(1):19-62. doi: 10.1038/kisup.2012.64.
8
Coding variants in nephrin (NPHS1) and susceptibility to nephropathy in African Americans.非洲裔美国人中nephrin(NPHS1)的编码变异与肾病易感性
Clin J Am Soc Nephrol. 2014 Aug 7;9(8):1434-40. doi: 10.2215/CJN.00290114. Epub 2014 Jun 19.
9
JK null alleles identified from Japanese individuals with Jk(a−b−) phenotype.从具有Jk(a−b−)表型的日本个体中鉴定出的JK无效等位基因。
Vox Sang. 2014 May;106(4):382-4. doi: 10.1111/vox.12117.
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APOL1 risk variants, race, and progression of chronic kidney disease.APOL1 风险变异体、种族与慢性肾脏病的进展。
N Engl J Med. 2013 Dec 5;369(23):2183-96. doi: 10.1056/NEJMoa1310345. Epub 2013 Nov 9.