The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity

Abstract

(2016) The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity. Kidney International, 90 (2). pp. 396-403. Permanent WRAP URL:http://wrap.warwick.ac.uk/78200 Copyright and reuse:The Warwick Research Archive Portal (WRAP) makes this work by researchers of the University of Warwick available open access under the following conditions. Copyright © and all moral rights to the version of the paper presented here belong to the individual author(s) and/or other copyright owners. To the extent reasonable and practicable the material made available in WRAP has been checked for eligibility before being made available.Copies of full items can be used for personal research or study, educational, or not-for-profit purposes without prior permission or charge. Provided that the authors, title and full bibliographic details are credited, a hyperlink and/or URL is given for the original metadata page and the content is not changed in any way. A note on versions:The version presented here may differ from the published version or, version of record, if you wish to cite this item you are advised to consult the publisher's version. Please see the 'permanent WRAP url' above for details on accessing the published version and note that access may require a subscription.For more information, please contact the WRAP Team at: wrap@warwick.ac.uk

Thiamine Diphosphate Status and Dialysis-Related Losses in End-Stage Kidney Disease Patients Treated with Hemodialysis

“…However, in view of high concentrations of oxythiamine, an antythiamine compound, reported recently in ESRD by Zhang et al [5], the reference concentrations of thiamine might not necessarily comply with its increased needs in hemodialysed patients. The astonishing lack of association between TDP levels and vitamin B1 intake reported in dietary recalls or between the presence or lack of vitamin B1 supplementation reflects either the prominent role of thiamine produced by gut microbiota in thiamine homeostasis or the impaired process of thiamine phosphorylation into TDP in ESRD.…”

“…Most data published so far analyzed serum values, or transketolase activity, which make unreliable reflections of vitamin B1 status in ESRD [5]. …”

“…Anorexia and insufficient dietary intake are regarded as the most important contributors [2,3]. However, new contributors have emerged recently, including impaired gastrointestinal absorption by specific transporters, or the role of microbiota in the production of thiamine antagonist, oxythiamine, both, importantly, influenced by ESRD [4,5]. …”

Functional thiamine deficiency in end-stage renal disease: malnutrition despite ample nutrients

“…Therefore, it is commonly acknowledged that uremic toxin(s) accumulating in patients with ESRD causes inhibition of transketolase activity, hence causing functional thiamine deficiency. The identity of the toxin(s) causing this abnormality was not definitively determined until the recent study by Zhang et al 5 (2016) that showed that plasma concentrations of oxythiamine, a well-known thiamine antagonist and inhibitor of transketolase, are significantly increased in patients with ESRD. Using liquid chromatography and mass spectrometry, Zhang et al analyzed plasma samples from patients with ESRD on hemodialysis and peritoneal dialysis and compared the results with those of healthy control subjects.…”

Acute Shoshin beriberi syndrome immediately post–kidney transplant with rapid recovery after thiamine administration

“…Micronutrient deficiency, however, is now uncommon in transplant recipients due to routine use of supplementation . In spite of this, accumulation of the uremic toxin oxythiamine can result in functional thiamine deficiency by competitively inhibiting transketolase activity …”