Clinical Chemistry AACC Online Job Center
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 40: 1544-1548, 1994;
This Article
Right arrow Full Text (PDF)
Right arrow Submit an electronic Letter to
the Editor about this paper
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by France, N. C.
Right arrow Articles by Wallace, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by France, N. C.
Right arrow Articles by Wallace, M. R.

Clinical Chemistry, Vol 40, 1544-1548, Copyright © 1994 by American Association for Clinical Chemistry

Contribution of dialysis to endogenous oxalate production in patients with chronic renal failure

NC France, PT Holland and MR Wallace
Department of Pathology, Waikato Hospital, Hamilton, New Zealand.

We tested the possibility that the buffering agents in dialysis bath fluid might contribute to increased endogenous oxalate production in dialyzed patients. Using stable isotope dilution mass spectrometry, we obtained oxalate production rates and pool sizes directly for 10 patients in chronic renal failure, 5 of whom were undergoing continuous ambulatory peritoneal dialysis (lactate-buffered fluid). All peritoneal dialysis patients had either increased oxalate production rates or expanded oxalate pools when compared with undialyzed patients in renal failure. From a further four patients receiving maintenance hemodialysis we took blood samples immediately before and after three consecutive dialysis sessions in which the bath-fluid buffering agent (bicarbonate or acetate) was alternated; we analyzed these samples for oxalate and key precursors by capillary gas chromatography. Plasma glycine and serine concentrations remained within the physiological range. Glycolate and oxalate concentrations decreased, but the oxalate remained above normal after dialysis. All changes were independent of the bath-fluid buffering agent. We suggest that dialysis might stimulate the formation of oxalate by removing product inhibition of a late catabolic step.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1994 by the American Association for Clinical Chemistry.