Relationship of nervous tissue transketolase to the neuropathy in chronic uremia

Sterzel, R. Bernd; Semar, M.; Lonergan, E. T.; Treser, Gerhard; Lange, Katharina

doi:10.1172/jci106727

Cited by 42 publications

(15 citation statements)

References 33 publications

(40 reference statements)

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“…In this study, no effect of vitamin B 1 supplementation on tHcy levels was shown in patients with homocystinuria due to cystathionine-␤ synthase deficiency. Lack of effect of thiamine supply on tHcy levels in renal failure may be related to the impairment of neural tissue transketolase (43) or erythrocyte transketolase activity (44), a potential indicator of thiamine deficiency, which was ascribed to low molecular weight uremic toxins in renal failure patients. In this context, Descombes et al (16) described an impaired basal erythrocyte transketolase activity despite normal thiamine plasma levels without improvement of transketolase activity after addition of thiamine in vitro in the majority of hemodialysis patients.…”

Section: Discussionmentioning

confidence: 99%

Riboflavin Is a Determinant of Total Homocysteine Plasma Concentrations in End-Stage Renal Disease Patients

Skoupy¹,

Födinger²,

Veitl³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. The effect of thiamine (vitamin B 1 ) or riboflavin (vitamin B 2 ) availability on fasting total homocysteine (tHcy) plasma levels in end-stage renal disease patients is unknown. A cross-sectional study was performed in a population of nonvitamin supplemented patients maintained on continuous ambulatory peritoneal dialysis. Red blood cell availability of thiamine (␣-ETK) and of riboflavin (␣-EGR), along with other predictors of tHcy plasma levels, was considered in the analysis. There was a linear association of ␣-EGR with tHcy plasma concentrations (P ϭ 0.009), which was not observed for ␣-ETK. Among red blood cell vitamins, ␣-EGR was the only predictor of tHcy levels (P ϭ 0.035), whereas ␣-ETK, red blood cell pyridoxal-5-phosphate supply (␣-EGOT) and red blood cell folate levels had no effect. The risk for having a high tHcy plasma levels within the fourth quartile (plasma tHcy Ͼ38.3 mol/L) was increased by an ␣-EGR Ͼ median (odds ratio, 4.706; 95% confidence interval, 1.124 to 19.704; P ϭ 0.026). By way of contrast, ␣-ETK had no effect in these analyses. Independent predictors of tHcy plasma levels were serum albumin, ␣-EGR, red blood cell folate, and certain MTHFR genotypes. A logistic regression analysis showed that the MTHFR genotype is a predictor for having a tHcy plasma concentration within the fourth quartile. In summary, riboflavin availability, as measured by ␣-EGR, is a determinant of fasting tHcy plasma levels in peritoneal dialysis patients. This finding may have implications for tHcy lowering therapy in individuals with end-stage renal disease.The majority of patients with impaired renal function present elevated total homocysteine (tHcy) plasma levels (1). Established predictors of tHcy plasma levels in the renal failure population include serum albumin and serum creatinine levels, creatinine clearance, folate status, vitamin B 12 and vitamin B 6 levels, as well as genetic variants in enzymes involved in the folate cycle or in the remethylation of homocysteine (2-7). An elevated tHcy plasma level can indicate folate and/or vitamin B 12 deficiency (8) and is associated with a variety of pathologic conditions such as vascular disease (9 -11) or birth defects (12). Although genetic and nongenetic factors have been shown to determine tHcy concentrations of patients with renal insufficiency, the cause of hyperhomocysteinemia among these patients is not completely understood (13).The role of B-group vitamins other than vitamin B 6 or vitamin B 12 as determinants of hyperhomocysteinemia in the general population and in the setting of renal insufficiency is far from clear, although vitamin B 1 (thiamine pyrophosphate) and vitamin B 2 (riboflavin) are involved in the metabolism of methionine and homocysteine.We assumed that thiamine or riboflavin availability is a predictor of fasting tHcy plasma levels in end-stage renal disease (ESRD). To test this hypothesis, we performed a crosssectional study among a population of non-vitamin supplemented patients maintained on continuous ambulatory perito...

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Section: Discussionmentioning

confidence: 99%

Riboflavin Is a Determinant of Total Homocysteine Plasma Concentrations in End-Stage Renal Disease Patients

Skoupy¹,

Födinger²,

Veitl³

et al. 2002

Journal of the American Society of Nephrology

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“…This enzyme was shown to be significantly inhibited by plasma, cerebrospinal fluid and low molecular weight (<500 dalton) dialysate fractions obtained from patients with uremic neuropathy, but not by samples from normal subjects [8] or with high level of uremia [9]. It is also of interest that in uremic subjects, TK activity of erythrocytes was found to be abnormal but it improves following dialytic therapy [6].…”

Section: Introductionmentioning

confidence: 99%

Acute encephalopathy in a person with spinal cord injury and chronic renal failure, treated with high doses of thiamine

Stampacchia¹,

Gerini²,

Gattai³

2018

Neurol Disord Therap

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Encephalopathy due to thiamine deficit is described mainly in alcohol addicted persons. Thiamine is one of the micronutrients that resulted deficient in patients with spinal cord injury (SCI), but no cases of acute encephalopathy due to thiamine deficit in SCI person is published. In this paper is reported an acute loss of consciousness in a person affected by sub-acute spinal cord injury (a spinal cord compression due to an hematoma), chronic renal failure (secondary to a nephrectomy for a widespread urinary bladder neoplasia and an atrophic contralateral kidney) in treatment by dialysis, and negative anamnesis for alcoholic abuse, recovered after four days of high doses of thiamine parenteral administration .

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“…6 This occurred in the presence of normal levels of plasma thiamine and red blood cell TPP. 4,7,8 The mechanism of reversible inhibition of transketolase in renal failure has remained unresolved for over 40 years.…”

mentioning

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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(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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Relationship of nervous tissue transketolase to the neuropathy in chronic uremia

Cited by 42 publications

References 33 publications

Riboflavin Is a Determinant of Total Homocysteine Plasma Concentrations in End-Stage Renal Disease Patients

Riboflavin Is a Determinant of Total Homocysteine Plasma Concentrations in End-Stage Renal Disease Patients

Acute encephalopathy in a person with spinal cord injury and chronic renal failure, treated with high doses of thiamine

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

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