title: An oral load of the early glycation compound lactuloselysine fails to accumulate in the serum of uraemic patients.
abstract: BACKGROUND
  It has been hypothesized that in renal failure, exogenous glycation compounds from food accumulate and play a major pathogenetic role when renal excretion is impaired.
  
  
  METHODS
  To address this, a diet containing a defined amount of the lysine Amadori product (AP) lactuloselysine was used. Plasma concentrations and cumulative urinary excretion of AP were assessed in 16 healthy subjects, 12 renal failure patients and 6 continuous ambulatory peitoneal dialysis (CAPD) patients. Amadori product was measured as furosine using reverse phase high performance liquid chromatography (RP-HPLC) after acid hydrolysis.
  
  
  RESULTS
  A diet low in glycation compounds significantly decreased excretion of APs in healthy subjects. In healthy individuals, ingestion of lactuloselysine bound to food proteins caused only a minor acute increase (8.24+/-1.11 mg/day, 2% of the administered dose) of AP excretion in the urine; in patients with renal failure not yet on dialysis, the increase in AP excretion in the urine was significantly less (4.0+/-0.51 mg/day) and the same was true in CAPD patients (0.21+/-0.09 mg/day). The plasma concentration of total APs, i.e. the sum of APs as free amino acids and residues bound to plasma proteins, did not change in any of the three groups, however.
  
  
  CONCLUSIONS
  Dietary APs do not accumulate in the blood even in advanced renal failure. The amount of APs measured as furosine excreted in the urine is significantly less, however, in renal failure and CAPD patients compared with healthy subjects. Although the findings exclude accumulation of lactuloselysine in renal failure, they do not generally exclude accumulation of other food-derived advanced glycation end products (AGEs).
authors.affiliation: Department of Nephrology, University of Heidelberg, Bergheimerstr. 56a, 69115 Heidelberg, Germany. vedat_schwenger@med.uni-heidelberg.de
authors.forename: Vedat
authors.initials: V
authors.lastname: Schwenger
authors.forename: Christian
authors.initials: C
authors.lastname: Morath
authors.forename: Kathrin
authors.initials: K
authors.lastname: Schönfelder
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Klein
authors.forename: Kai
authors.initials: K
authors.lastname: Weigel
authors.forename: Reinhold
authors.initials: R
authors.lastname: Deppisch
authors.forename: Thomas
authors.initials: T
authors.lastname: Henle
authors.forename: Eberhard
authors.initials: E
authors.lastname: Ritz
authors.forename: Martin
authors.initials: M
authors.lastname: Zeier
mesh_terms: D000284:Administration, Oral; D006031:Glycosylation; D006801:Humans; D007792:Lactulose / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism; D010531:Peritoneal Dialysis, Continuous Ambulatory; D051437:Renal Insufficiency / Q000097:blood* / Q000150:complications / Q000378:metabolism / Q000628:therapy; D014511:Uremia / Q000097:blood* / Q000209:etiology / Q000378:metabolism
chemical_list: C040454:epsilon-N-1-(1-deoxylactulosyl)lysine; D007792:Lactulose