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 An erratum has been published
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 Google Scholar
Google Scholar
Right arrow Articles by Lipkin, E. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lipkin, E. W.
Agricola
Right arrow Articles by Lipkin, E. W.

American Journal of Clinical Nutrition, Vol 67, 246-254, Copyright © 1998 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

A longitudinal study of calcium regulation in a nonhuman primate model of parenteral nutrition

EW Lipkin
Department of Medicine, University of Washington, Seattle 98195-6426, USA.

The question of whether parenteral nutrition adversely affects calcium regulation remains unclear. Human studies of this question have been confounded by uncontrolled variables including the degree to which food is ingested orally; gut absorption; underlying disease; medication adversely affecting bone, including steroids; and aluminum contamination of parenteral nutrients. The present study was undertaken to examine whether parenteral nutrition adversely affects calcium regulation in a nonhuman primate model that allows for control of underlying clinical variables and mobility. With use of this model, it was possible to show weight maintenance and positive nitrogen and calcium balances with parenteral nutrition. There was no demonstrable effect of the animals' wearing a jacket and tether system or of catheterization on calcium regulation. Calciuria in response to parenteral nutrition was elevated initially but diminished by 2 wk of therapy. The calciuria observed resulted from an increased urine- filtered calcium load. Calcium balance with parenteral nutrition was preserved by a diminished fraction of calcium filtered by the kidney being excreted in the urine. The present study suggests that negative calcium balance produced by parenteral nutrition may result from abnormal renal tubular function or disruption of normal parathyroid hormone regulation.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 by The American Society for Nutrition