title: Hyperhomocysteinemia confers an independent increased risk of atherosclerosis in end-stage renal disease and is closely linked to plasma folate and pyridoxine concentrations.
abstract: BACKGROUND
  A high level of total plasma homocysteine is a risk factor for atherosclerosis, which is an important cause of death in renal failure. We evaluated the role of this as a risk factor for vascular complications of end-stage renal disease.
  
  
  RESULTS
  Total fasting plasma homocysteine and other risk factors were documented in 176 dialysis patients (97 men, 79 women; mean age, 56.3 +/- 14.8 years). Folate, vitamin B12, and pyridoxal phosphate concentrations were also determined. The prevalence of high total homocysteine values was determined by comparison with a normal reference population, and the risk of associated vascular complications was estimated by multiple logistic regression. Total homocysteine concentration was higher in patients than in the normal population (26.6 +/- 1.5 versus 10.1 +/- 1.7 mumol/L; P < .01). Abnormally high concentrations (> 95th percentile for control subjects, 16.3 mumol/L) were seen in 149 patients (85%) with end-stage renal disease (P < .001). Patients with a homocysteine concentration in the upper two quintiles (> 27.8 mumol/L) had an independent odds ratio of 2.9 (CI, 1.4 to 5.8; P = .007) of vascular complications. B vitamin levels were lower in patients with vascular complications than in those without. Vitamin B6 deficiency was more frequent in patients than in the normal reference population (18% versus 2%; P < .01).
  
  
  CONCLUSIONS
  A high total plasma homocysteine concentration is an independent risk factor for atherosclerotic complications of end-stage renal disease. Such patients may benefit from higher doses of B vitamins than those currently recommended.
authors.affiliation: Department of Cardiology, Cleveland Clinic Foundation, OH 44195, USA. robinsk@ccsmtp.ccf.org
authors.forename: K
authors.initials: K
authors.lastname: Robinson
authors.forename: A
authors.initials: A
authors.lastname: Gupta
authors.forename: V
authors.initials: V
authors.lastname: Dennis
authors.forename: K
authors.initials: K
authors.lastname: Arheart
authors.forename: D
authors.initials: D
authors.lastname: Chaudhary
authors.forename: R
authors.initials: R
authors.lastname: Green
authors.forename: P
authors.initials: P
authors.lastname: Vigo
authors.forename: E L
authors.initials: EL
authors.lastname: Mayer
authors.forename: J
authors.initials: J
authors.lastname: Selhub
authors.forename: M
authors.initials: M
authors.lastname: Kutner
authors.forename: D W
authors.initials: DW
authors.lastname: Jacobsen
mesh_terms: D000368:Aged; D000375:Aging / Q000097:blood; D001161:Arteriosclerosis / Q000209:etiology*; D005260:Female; D005492:Folic Acid / Q000097:blood*; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D009994:Osmolar Concentration; D010531:Peritoneal Dialysis, Continuous Ambulatory; D011736:Pyridoxine / Q000097:blood*; D006435:Renal Dialysis; D012307:Risk Factors; D017678:Sex Distribution; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D006710:Homocysteine; D005492:Folic Acid; D011736:Pyridoxine; D014805:Vitamin B 12