NDT Advance Access originally published online on October 4, 2005
Nephrology Dialysis Transplantation 2006 21(2):383-388; doi:10.1093/ndt/gfi151
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Clinical Nephrology
An oral load of the early glycation compound lactuloselysine fails to accumulate in the serum of uraemic patients
1 Department of Nephrology, University of Heidelberg, Heidelberg, Germany, 2 Gambro Corporate Research, Hechingen, Germany and 3 Institute of Food Chemistry, Technische Universität Dresden, Dresden, Germany
Correspondence and offprint requests to: Vedat Schwenger, MD, Department of Nephrology, University of Heidelberg, Bergheimerstr. 56a, 69115 Heidelberg, Germany. Email: vedat_schwenger{at}med.uni-heidelberg.de
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.
Conclusion. 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).
Keywords: advanced glycation end products (AGEs); furosine; lactuloselysine; nutrition; renal failure
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