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血管紧张素转换酶基因多态性与肝肾综合征的相关性研究

[Correlative study between angiotensin-converting enzyme gene polymorphism and hepatorenal syndrome].

作者信息

Wu Xi-xin, Zheng Zhi-xiong, Liu Zhong-liang, Zhou Yu-qiu, Xiao Ge-fei, Peng Jian, Zeng Zhi-wei

机构信息

Department of Nephrology, The Fifth Affiliated Hospital, Zhongshan University, Zhuihai 519000, Guangdong, China.

出版信息

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2005 Feb;17(2):121-3.

Abstract

OBJECTIVE

To investigate the relationship between insertion/deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE) gene and uncompensated cirrhosis of liver with hepatorenal syndrome (HRS).

METHODS

ACE I/D polymorphism was detected by polymerase chain reaction amplification of DNA fragment in 56 patients of uncompensated liver cirrhosis with HRS, and 60 healthy individuals served as the controls. At the same time, alanine aminotransferase, aspartate transaminase, serum creatinine (SCr), blood urea nitrogen (BUN) and glomerular filtration rate (GFR) etc. were measured in all the subjects, and the difference between these variables among different genotypes was noted.

RESULTS

There was no significant difference in genotypes and allele frequency between the HRS group and controls(all P>0.05). The I allele frequency was higher than the D allele in all the subjects (all P<0.01). But in the control group, there was no significant difference in the genotype frequency among three genomic groups, while the II genotype frequency was higher than the one of ID and DD (all P<0.05). SCr and BUN of the II genotype were higher in the HRS group than that of ID and DD(both P<0.05) and GFR of the II genotype was lower than the one of ID and DD in the HRS group(P<0.05).

CONCLUSION

There is relationship between ACE gene polymorphism and the incidence of uncompensated liver cirrhosis with HRS. II genotype may be the genetic factor of vulnerability to HRS patients with uncompensated cirrhosis of liver. The degree of kidney failure in II genotype population is more serious than in ID and DD individuals with uncompensated liver cirrhosis complicated by HRS.

摘要

目的

探讨血管紧张素转换酶(ACE)基因插入/缺失(I/D)多态性与失代偿期肝硬化合并肝肾综合征(HRS)的关系。

方法

采用聚合酶链反应扩增DNA片段的方法,检测56例失代偿期肝硬化合并HRS患者及60例健康对照者的ACE I/D多态性。同时,测定所有研究对象的丙氨酸氨基转移酶、天冬氨酸氨基转移酶、血清肌酐(SCr)、血尿素氮(BUN)及肾小球滤过率(GFR)等指标,并比较不同基因型各指标的差异。

结果

HRS组与对照组的基因型及等位基因频率差异均无统计学意义(均P>0.05)。所有研究对象中I等位基因频率均高于D等位基因(均P<0.01)。对照组中,三种基因分组的基因型频率差异无统计学意义,但II基因型频率高于ID和DD基因型(均P<0.05)。HRS组中,II基因型患者的SCr和BUN均高于ID和DD基因型患者(均P<0.05),而II基因型患者的GFR低于ID和DD基因型患者(P<0.05)。

结论

ACE基因多态性与失代偿期肝硬化合并HRS的发病有关。II基因型可能是失代偿期肝硬化合并HRS患者发生肝肾综合征的易感基因因素。失代偿期肝硬化合并HRS的II基因型人群肾衰竭程度较ID和DD基因型人群更严重。

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