Effect of chronic kidney disease on the expression of thiamin and folic acid transporters

Bukhari, Farhan J.; Moradi, Hamid Reza; Gollapudi, Pavan; Kim, Hyun Ju; Vaziri, Nosratola D.; Said, Hamid M.

doi:10.1093/ndt/gfq675

Cited by 54 publications

(31 citation statements)

References 49 publications

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“…36 Further disturbance of thiamine metabolism in renal failure occurs by decreased expression of thiamine transporters in small intestine, heart, liver and brain and likely decreased availability of thiamine at these sites. 37 Herein we showed that incubation of red blood cells from HD patients ex vivo with thiamine restored normal levels of transketolase activity and R5P concentration, consistent with correction of impaired pentose pathway activity.…”

supporting

confidence: 59%

“…Recent studies in diabetes and CKD suggest there are also abnormalities of thiamine transport due to tissue-specific down regulation of thiamine transporters. 14,37,47 Measurement of renal clearance of thiamine is a sensitive clinical marker of this. 14 Red blood cell transketolase activity is valuable to assess impact on the pentosephosphate pathway and αETKA to explore cause of transketolase activity deficit.…”

Section: In Clinical Translation Dietary Deficiency Of Thiamine -Leamentioning

confidence: 99%

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

Zhang

Masania

Anwar

et al. 2016

Kidney International

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(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

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supporting

confidence: 59%

Section: In Clinical Translation Dietary Deficiency Of Thiamine -Leamentioning

confidence: 99%

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

Zhang

Masania

Anwar

et al. 2016

Kidney International

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“…These microvascular pathologies, such as thrombosis, are mediated by inflammatory, atherogenic, and oxidative mechanisms. 18,21 Furthermore, clinical changes observed in patients with CKD, such as low intracellular levels of folate and thiamine, 22 or aberrant nitric oxide metabolism, 23 can increase susceptibility to cerebral infarction and white matter hyper-intensities (lesions) in the brain ( Figure 1, Table 1). 21,23 Small vessel disease (SVD) is a pathological process that affects the arterioles, venules, and capillaries, causing ischaemic or haemorrhagic lesions.…”

Section: Microvascular Diseasementioning

confidence: 99%

Kidney–brain crosstalk in the acute and chronic setting

et al. 2015

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Patients with kidney disease often exhibit multiple organ dysfunction that is caused, in part, by marked connectivity between the kidney and other organs and tissues. Substantial crosstalk occurs between the kidney and the brain, as indicated by the frequent presentation of neurological disorders, such as cerebrovascular disease, cognitive impairment, and neuropathy during the natural history of chronic kidney disease. The underlying pathophysiology of such comorbid neurological disorders in kidney disease is governed by shared anatomic and vasoregulatory systems and humoral and non-humoral bidirectional pathways that affect both the kidney and the brain. During acute kidney injury, the brain and kidney might interact through the amplification of cytokine-induced damage, extravasation of leukocytes, oxidative stress, and dysregulation of sodium, potassium, and water channels. The advent of dialysis and renal transplantation programmes has led to a reduction in the rate of neurological complications associated with uraemia, but a new set of complications have arisen as a consequence of the effects of dialysis on the central nervous system over the short and long term. This Review discusses the clinical complications of acute and chronic renal failure from a neurologic perspective, and highlights current understanding of the underlying pathophysiologies.

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“…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]. …”

Section: Introductionmentioning

confidence: 99%

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

et al. 2017

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Aim: (1) To describe the whole blood content of thiamine diphosphate (TDP), a biologically active form of vitamin B1 in end-stage kidney disease patients treated with hemodialysis (HD); (2) to establish the impact of a single HD procedure on TDP blood concentrations; and (3) to describe potential explanatory variables influencing TDP dialysis related losses, including dialysis prescription, vitamin B1 dietary intake and supplementation. Methods: Single-center, cross-sectional study in 50 clinically stable maintenance HD patients. The assessment of whole blood TDP with the High Performance Liquid Chromatography method, before and after a single, middle-week dialysis session and analysis of clinical and laboratory parameters potentially influencing TDP status Results: We report a significant difference in TDP levels before and after HD sessions - 42.5 (95% CI 38.7-46.2) μg/L and 23.6 (95% CI 18.9-28.2) μg/L, respectively (p = 0.000). The magnitude of intradialytic TDP changes is highly variable among individuals and is negatively associated only with the body weight of the patients (p < 0.013). Vitamin B1 dietary intake and supplementation do not influence whole blood TDP and dialysis-related loss of TDP. Conclusions: TDP, a bioactive compound of vitamin B1, is substantially lost during the HD procedure, and the magnitude of its loss is associated with the patient's body weight but it is not influenced by vitamin B1 dietary intake and standard supplementation dose.

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Effect of chronic kidney disease on the expression of thiamin and folic acid transporters

Cited by 54 publications

References 49 publications

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

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

Kidney–brain crosstalk in the acute and chronic setting

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

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