Skip Navigation



NDT Advance Access published online on October 4, 2005

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfi151
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
21/2/383    most recent
gfi151v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schwenger, V.
Right arrow Articles by Zeier, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schwenger, V.
Right arrow Articles by Zeier, M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received April 2, 2005
Accepted August 26, 2005


Orginal Article

An oral load of the early glycation compound lactuloselysine fails to accumulate in the serum of uraemic patients

Vedat Schwenger 1*, Christian Morath 1, Kathrin Schönfelder 2, Wolfgang Klein 1, Kai Weigel 2, Reinhold Deppisch 3, Thomas Henle 2, Eberhard Ritz 1, and Martin Zeier 1

1 Department of Nephrology, University of Heidelberg, Heidelberg, Germany
2 Institute of Food Chemistry, Technische Universität Dresden, Dresden, Germany
3 Gambro Corporate Research, Hechingen, Germany

* To whom correspondence should be addressed.
Vedat Schwenger, E-mail: vedat_schwenger{at}med.uni-heidelberg.de



  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.

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.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Nephrol Dial TransplantHome page
C. P. Schmitt, D. von Heyl, S. Rieger, K. Arbeiter, K. E. Bonzel, M. Fischbach, J. Misselwitz, A.-K. Pieper, F. Schaefer, and for the Mid European Pediatric Peritoneal Dialysis
Reduced systemic advanced glycation end products in children receiving peritoneal dialysis with low glucose degradation product content
Nephrol. Dial. Transplant., July 1, 2007; 22(7): 2038 - 2044.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.