AJCN North Carolina Research Campus
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Saito, A.
Right arrow Articles by Ohta, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Saito, A.
Right arrow Articles by Ohta, K.
Agricola
Right arrow Articles by Saito, A.
Right arrow Articles by Ohta, K.

American Journal of Clinical Nutrition, Vol 33, 1402-1406, Copyright © 1980 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Tryptophan and indolic tryptophan metabolites in chronic renal failure

A Saito, T Niwa, K Maeda, K Kobayashi, Y Yamamoto and K Ohta

Tryptophan and indolic tryptophan metabolites were measured in the serum of normal subjects and chronic renal failure patients. The tryptophan free/total ratio was 0.07 in the normal serum, but the other tryptophan metabolite values were below detectable levels. The free/total ratio was 0.66 in patients with chronic renal failure, and both increase of free tryptophan and decrease of total tryptophan were observed. At the same time, 5-hydroxyindoleacetic acid, indole acetic acid, 5-hydroxytryptophol, and N-acetyltryptophan also increased in the serum of chronic renal failure patients, existing not only in free form but in protein-bound form. In the serum samples, following hemodialysis the indolic tryptophan metabolites showed a tendency to decrease, and the tryptophan free/total ratio of 0.42 a approached the normal value. When indolic tryptophan metabolites were added to normal serum in vitro, the free tryptophan level rose, and competition for binding to albumin between tryptophan and indolic tryptophan metabolites was observed. These findings suggested that the cause of the decrease in protein-bound tryptophan in uremic serum may be an accumulation of indolic tryptophan metabolites which complete for binding to albumin in uremia.


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
G. Lesaffer, R. De Smet, N. Lameire, A. Dhondt, P. Duym, and R. Vanholder
Intradialytic removal of protein-bound uraemic toxins: role of solute characteristics and of dialyser membrane
Nephrol. Dial. Transplant., January 1, 2000; 15(1): 50 - 57.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1980 by The American Society for Nutrition