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

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

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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Female
  • Gene Deletion
  • Gene Frequency
  • Genotype
  • Hepatorenal Syndrome / genetics*
  • Humans
  • Male
  • Middle Aged
  • Mutagenesis, Insertional
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*

Substances

  • Peptidyl-Dipeptidase A