Association between polymorphisms in the renin-angiotensin system genes and prevalence of spontaneously aborted fetuses

Am J Reprod Immunol. 2013 Sep;70(3):238-45. doi: 10.1111/aji.12110. Epub 2013 Mar 11.

Abstract

Problem: The renin-angiotensin system is associated with angiogenesis, tissue remodeling, prenatal development, and Th2 cytokine production. The purpose of this study was to evaluate whether polymorphisms in angiotensin I-converting enzyme [ACE insertion/deletion (I/D)], angiotensinogen (AGT M235T), and angiotensin II type 1 receptor (AT1R 1166A>C) affect the prevalence of spontaneously aborted fetuses (SAFs).

Method of study: One hundred and ninety-eight SAFs were <20 weeks of gestational age. The control subjects were 103 healthy children and 640 adults collected from a convenience sample. Polymerase chain reaction and restriction fragment length polymorphism analysis were performed to identify the ACE I/D, AGT M235T, and AT1R 1166A>C genotypes.

Results: II/MM/AA, II/MT/AA, and II/TT/AC of ACE/AGT/AT1R were significantly different from controls. In particular, the statistical significance of the II/MM/AA genotype remained strong in chromosomally normal SAFs.

Conclusion: Our data suggest that the II/MM/AA of ACE/AGT/AT1R is a possible predisposing factor for spontaneous abortion.

Keywords: Polymorphism; renin-angiotensin system; spontaneous abortion; spontaneously aborted fetuses.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aborted Fetus
  • Abortion, Spontaneous / epidemiology*
  • Abortion, Spontaneous / genetics
  • Adolescent
  • Angiotensinogen / genetics*
  • Child
  • Child, Preschool
  • Female
  • Humans
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*
  • Polymorphism, Restriction Fragment Length
  • Pregnancy
  • Prevalence
  • Receptor, Angiotensin, Type 1 / genetics*
  • Renin-Angiotensin System / genetics*
  • Risk Factors

Substances

  • Receptor, Angiotensin, Type 1
  • Angiotensinogen
  • Peptidyl-Dipeptidase A