title: Glycoxidation and inflammation in renal failure patients.
abstract: BACKGROUND
  Inflammation is common in patients with chronic renal failure and has been associated with the increased risk for cardiovascular disease (CVD) in this condition. Advanced glycoxidation end products (AGEs) are among the factors implicated in the inflammatory state of chronic renal failure.
  
  
  METHODS
  In a cross-sectional study of 189 dialysis patients, we measured circulating levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), vascular adhesion molecule-1 (VCAM-1), vascular endothelial growth factor (VEGF), and plasminogen activator inhibitor-1 (PAI-1) to test for possible relationships between them and serum AGE levels. In addition, these parameters were measured in a subgroup of 18 patients with chronic renal failure randomly assigned to a 4-week diet, either low (L-AGE) or high (H-AGE) in AGE content. AGEs were measured by means of a monoclonal antibody against epsilonN-carboxymethyllysine.
  
  
  RESULTS
  At baseline, serum AGE levels, as well as those for CRP, TNF-alpha, VCAM-1, and VEGF, were markedly elevated, although no correlation was found between AGE levels and the other markers. Dietary AGE modulation resulted in a significant decrease in levels of serum AGEs, CRP, and PAI-1 in the L-AGE group (approximately 35%, 44%, and 17%, respectively; P < 0.03), whereas only serum AGE levels increased significantly in the H-AGE group. VCAM-1 and TNF-alpha levels, although similar at baseline, became significantly lower in patients on an L-AGE compared with H-AGE diet (P < 0.05) at the end of the study.
  
  
  CONCLUSIONS
  Data from the interventional phase of the study suggest that AGEs have a role in the initiation of the inflammatory state of chronic renal failure, which eventually leads to increased CVD. This finding opens the possibility for using anti-AGE strategies in the prevention and treatment of CVD in patients with chronic renal failure.
authors.affiliation: Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029, USA.
authors.forename: Melpomeni
authors.initials: M
authors.lastname: Peppa
authors.forename: Jaime
authors.initials: J
authors.lastname: Uribarri
authors.forename: Weijing
authors.initials: W
authors.lastname: Cai
authors.forename: Min
authors.initials: M
authors.lastname: Lu
authors.forename: Helen
authors.initials: H
authors.lastname: Vlassara
mesh_terms: D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D003430:Cross-Sectional Studies; D004032:Diet; D005260:Female; D017127:Glycation End Products, Advanced / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000209:etiology; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D051437:Renal Insufficiency / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D012189:Retrospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D017127:Glycation End Products, Advanced; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D002097:C-Reactive Protein