title: Association of apolipoprotein E gene polymorphism with end-stage renal disease and hyperlipidemia in patients on long-term hemodialysis.
abstract: BACKGROUND
  Cardiovascular diseases (CVDs) are the leading cause of death of patients with chronic renal failure. Apolipoprotein E (apoE) plays an important role in the homeostasis of cholesterol and triglycerides.
  
  
  OBJECTIVE
  We aimed to investigate the possible link(s) between apoE gene polymorphism, inflammation and lipoproteins in hemodialysis patients.
  
  
  METHODS
  We studied 109 end-stage renal disease (ESRD) patients and 97 controls. The serum lipids, apolipoproteins, lipoprotein particles, high-sensitivity C-reactive protein (hs-CRP) and total homocysteine (t-Hcy) levels and paraoxonase (PON) activity were determined in our patients. We also analyzed apoE gene polymorphism in the patients and controls.
  
  
  RESULTS
  The analysis of the apoE gene demonstrated a predominance of the e3 allele in both the patients and controls, followed by the e4 and then the e2 alleles. The analysis of the apoE genotype and allele frequencies showed significantly higher e4 allele and E3E4 genotype frequencies and decreased e3 allele and E3E3 genotype frequencies in the patients compared with the controls. The e2, e4 and E3E4 carriers within the ESRD patient population presented an atherogenic lipid profile. However, there were no significant variations in the serum PON activity and the hs-CRP and t-Hcy levels between individuals with different apoE polymorphisms.
  
  
  CONCLUSIONS
  Our findings suggest an association between the e4 allele, E3E4 genotype and ESRD. The apoE polymorphism affects the serum lipoprotein levels, and the ESRD patients who are e4 and e2 allele carriers are more likely to present an atherogenic lipoprotein profile that may be a major factor associated with increased risk of CVD.
authors.affiliation: Faculty of Sciences Ben M'sik, Laboratory of Biology and Health, Hassan II University , Casablanca , Morocco .
authors.forename: Hanaâ
authors.initials: H
authors.lastname: Lahrach
authors.forename: Fadwa
authors.initials: F
authors.lastname: Essiarab
authors.forename: Mohammed
authors.initials: M
authors.lastname: Timinouni
authors.forename: Bachir
authors.initials: B
authors.lastname: Hatim
authors.forename: Salma
authors.initials: S
authors.lastname: El Khayat
authors.forename: Loubna
authors.initials: L
authors.lastname: Er-Rachdi
authors.forename: Jamal
authors.initials: J
authors.lastname: Jarir
authors.forename: Anas
authors.initials: A
authors.lastname: Kettani
authors.forename: Noreddine
authors.initials: N
authors.lastname: Ghalim
authors.forename: Hassan
authors.initials: H
authors.lastname: Taki
authors.forename: Halima
authors.initials: H
authors.lastname: Lebrazi
authors.forename: Benyounes
authors.initials: B
authors.lastname: Ramdani
authors.forename: Rachid
authors.initials: R
authors.lastname: Saïle
mesh_terms: D000328:Adult; D001057:Apolipoproteins E / Q000235:genetics*; D016022:Case-Control Studies; D005787:Gene Frequency; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000235:genetics* / Q000628:therapy; D050356:Lipid Metabolism / Q000235:genetics*; D008055:Lipids / Q000097:blood*; D008875:Middle Aged; D011110:Polymorphism, Genetic; D006435:Renal Dialysis
chemical_list: D001057:Apolipoproteins E; D008055:Lipids
keywords: ApoE polymorphism; apolipoproteins; cardiovascular risk; end-stage renal disease; inflammation; lipids