title: [Increased levels of circulating advanced glycation end products in a model of acute renal insufficiency in rats].
abstract: BACKGROUND
  Advanced glycation end products (AGEs) are formed from proteins and peptides by non-enzymatic glycation or glycooxidation. AGEs are formed slowly during aging, and they accumulate in circulation and tissues in diabetes and chronic renal failure. Kidney plays a key role in the disposal of AGEs. Aim of this study was to verify the hypothesis that, acute loss of renal function with enhanced oxidative and carbonyl stress should result in a rise of circulating AGEs levels.
  
  
  RESULTS
  Acute renal failure (ARI) was induced in rats by bilateral nephrectomy (24-72 hours). The data on AGEs levels, oxidative status and antioxidative defense was compared to those of sham operated animals. 48 hours after the induction of ARI concentrations of AGEs, determined fluorimetrically or as carboxymethyllysine, rose 2-fold, and they correlated with concentrations of creatinine (r = 0.938, p < 0.001 and r = 0.815, p < 0.001, respectively). Malondialdehyde (MDA) and lipofuscine (LF) concentrations rose in a time dependent manner, suggesting an enhanced oxidative and carbonyl stress. Enhanced lipid peroxidation did not result from the suppressed antioxidant defense: activity of superoxide dismutase rose by 50%, while that of glutathione peroxidase was not compromised. Total antioxidant status increased, probably due to the accumulation of uremic toxins with scavenging capacity, such as hyppurate.
  
  
  CONCLUSIONS
  According to our knowledge our data was first to show a rapid increase in circulating AGEs concentrations in the model of acute renal failure in rats. If AGEs accumulate in acute renal failure in humans, their contribution to acute toxicity, and/or to the development of later complications, might be of a great importance.
authors.affiliation: Lekárska fakulta Univerzity Komenského, Bratislava.
authors.forename: P
authors.initials: P
authors.lastname: Boor
authors.forename: P
authors.initials: P
authors.lastname: Bozek
authors.forename: P
authors.initials: P
authors.lastname: Blazícek
authors.forename: D
authors.initials: D
authors.lastname: Syrová
authors.forename: R
authors.initials: R
authors.lastname: Schinzel
authors.forename: A
authors.initials: A
authors.lastname: Heidland
authors.forename: A
authors.initials: A
authors.lastname: Pecovová
authors.forename: K
authors.initials: K
authors.lastname: Sebeková
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D017127:Glycation End Products, Advanced / Q000097:blood*; D008062:Lipofuscin / Q000097:blood; D008239:Lysine / Q000031:analogs & derivatives / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D017127:Glycation End Products, Advanced; D008062:Lipofuscin; D008315:Malondialdehyde; C048496:N(6)-carboxymethyllysine; D003404:Creatinine; D008239:Lysine