title: Does hepatitis C increase the accumulation of advanced glycation end products in haemodialysis patients?
abstract: BACKGROUND
  Hepatitis C may cause increased levels of oxidative stress that contribute to accumulation of advanced glycation end products (AGEs), which increase the risk of cardiovascular disease (CVD). The aim of this study was to determine the influence of hepatitis C on AGE accumulation in haemodialysis patients.
  
  
  METHODS
  AGE accumulation was measured by means of skin autofluorescence (AF) in 92 haemodialysis (HD) patients and 93 age-matched healthy controls. In the HD patients, CVD-related biochemical variables were also measured. The HD patients were tested for hepatitis C virus (HCV) antibodies and allocated to a HCV+ or HCV- group.
  
  
  RESULTS
  Skin AF of the healthy subjects was lower than skin AF in the HD patients (3.13 +/- 0.95 vs 2.2 +/- 0.47; P < 0.001). We calculated the average increase of skin AF in the healthy subjects to be 0.017 arbitrary units per year, being 14 times lower than in HD patients with CVD only and 20 times lower than in HD patients suffering from combined CVD and diabetes mellitus (DM). Multivariate regression analysis showed that AGE accumulation in HD patients can be described by the independent effects of age, DM, CVD and HD vintage. Although inter-cellular adhesion molecule 1 and liver enzymes were elevated in HCV+ HD patients, levels of oxidative stress markers and skin AF were not significantly different between HCV+ and HCV- HD patients.
  
  
  CONCLUSIONS
  AGE accumulation was higher in the HD patients than in the healthy controls. AGE accumulation did not differ in HCV+ and HCV- HD patients. This might be due to the fact that hepatitis C did not cause oxidative stress in our HD population. Independent markers of AGE accumulation were age, HD vintage, DM and CVD, but not hepatitis C.
authors.affiliation: Department of Biomedical Engineering, University of Groningen, Groningen, The Netherlands.
authors.forename: Stefan
authors.initials: S
authors.lastname: Arsov
authors.forename: Reindert
authors.initials: R
authors.lastname: Graaff
authors.forename: Aurora M
authors.initials: AM
authors.lastname: Morariu
authors.forename: Wim
authors.initials: W
authors.lastname: van Oeveren
authors.forename: Andries J
authors.initials: AJ
authors.lastname: Smit
authors.forename: Irena
authors.initials: I
authors.lastname: Busletic
authors.forename: Lada
authors.initials: L
authors.lastname: Trajcevska
authors.forename: Gjulsen
authors.initials: G
authors.lastname: Selim
authors.forename: Pavlina
authors.initials: P
authors.lastname: Dzekova
authors.forename: Bernd
authors.initials: B
authors.lastname: Stegmayr
authors.forename: Aleksandar
authors.initials: A
authors.lastname: Sikole
authors.forename: Gerhard
authors.initials: G
authors.lastname: Rakhorst
mesh_terms: D000367:Age Factors; D000368:Aged; D002318:Cardiovascular Diseases / Q000150:complications; D016022:Case-Control Studies; D048909:Diabetes Complications / Q000150:complications; D005260:Female; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006526:Hepatitis C / Q000150:complications* / Q000276:immunology; D018937:Hepatitis C Antibodies / Q000097:blood; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D008099:Liver / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology; D012044:Regression Analysis; D006435:Renal Dialysis; D012307:Risk Factors; D012867:Skin / Q000378:metabolism
chemical_list: D017127:Glycation End Products, Advanced; D018937:Hepatitis C Antibodies