ACLS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
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 Levinson, D.
Right arrow Articles by Sorensen, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Levinson, D.
Right arrow Articles by Sorensen, L.
Annals of Clinical and Laboratory Science, Vol 12, Issue 1, 73-77
Copyright © 1982 by Association of Clinical Scientists

Articles

Renal handling of uric acid in man

DJ Levinson, DE Decker, and LB Sorensen

The uricosuric response to 80 mg of micronized Benzbromarone was employed to assess the renal tubular secretory site for uric acid in patients with primary gout. Since Benzbromarone selectively inhibits tubular reabsorption of secreted urate, the maximum uricosuria induced by this drug can be equated with the minimal secretory rate. Furthermore, a significant relationship was noted in normal controls between urate secretion and the plasma urate concentration (r = 0.956, p less than 0.005). Using the Benzbromarone response as a measure of tubular secretion, gouty patients with normal production hyperuricemia had a significantly lower secretory rate by comparison to patients with overproduction of uric acid. These data indicate that in patients with primary normal production hyperuricemia, the renal tubular defect is related to a decreased secretory response for a given plasma concentration of uric acid.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1982 by the Association of Clinical Scientists.