血管紧张素转换酶基因多态性与肝肾综合征相关研究

目的　探讨血管紧张素转换酶 (ACE)基因插入 /缺失 (I/ D)多态性与失代偿性肝硬化并发肝肾综合征 (HRS)之间的关系。方法　应用聚合酶链反应方法扩增 5 6例失代偿性肝硬化并发 HRS患者及 6 0例正常对照组 ACE基因上 DNA片断 ,根据 I/ D判断其多态性 ;同时各例均采血测丙氨酸转氨酶、天冬氨酸转氨酶、血清肌酐 (SCr)及尿素氮 (BU N)等指标 ,并测定肾小球滤过率 (GFR) ,比较不同基因型间上述指标的差异显著性。结果　 HRS患者各基因型及等位基因频率与对照组间差异均无显著性 (P均 >0 .0 5 ) ;I等位基因频率均显著高于 D等位基因频率 (P均 <0 .0 1)。正常对照组中 3种基因型频率间差异无显著性 (P>0 .0 5 ) ;HRS组中 II基因型频率显著高于 ID型及 DD型 (P均 <0 .0 5 )。 II基因型的 BU N与 SCr均显著高于 ID型及 DD型(P均 <0 .0 5 ) ,GFR显著低于 ID型及 DD型 (P均 <0 .0 5 )。结论　 ACE基因多态性与失代偿性肝硬化并发HRS的发生率有关 ,II基因型可能为失代偿性肝硬化易并发 HRS的遗传学方面因素 ;失代偿性肝硬化并发HRS患者中 ,II基因型个体的肾功能衰竭程度重于 ID型及 DD型。

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

Objective To investigate the relationship between insertion/deletion(I/D) polymorphism of angiotensinconverting 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 hepatocirrhosis 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 hepatocirrhosis 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 hepatocirrhosis complicated by HRS.