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Special Issue "The Intestine and Uremia"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Uremic Toxins".

Deadline for manuscript submissions: closed (30 June 2018)

Special Issue Editor

Guest Editor
Prof. Dr. Griet Glorieux

Department of Internal Medicine, Nephrology Division, Ghent University Hospital, 9000 Ghent, Belgium
E-Mail
Interests: Uremic toxins; Protein binding; Chronic kidney disease; Leukocyte/monocyte function; Leukocyte-Endothelial interaction; Inflammation in CKD; Dialysis fluid purity/endotoxin; Gut-kidney axis

Special Issue Information

Dear Colleagues,

The interaction between the host and the intestinal microbiota has recently been a focus of increasing interest. In chronic kidney disease (CKD), the interaction is bidirectional, while uremia affects both the composition and the metabolism of the intestinal microbiota, important uremic toxins are generated by the microbial metabolism. In addition, intestinal dysbiosis leads to a disruption of the intestinal barrier function, contributing to inflammation. The predominant proteolytic fermentation pattern in CKD contributes to the generation of well-known uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, both end-products of protein fermentation, of which the cardiovascular and renal toxicity has been demonstrated extensively in in vitro, in vivo (animal) and clinical studies. In order to be able to target these, and other, intestinally generated toxins, a better characterization of the intestinal microbial profile in CKD is needed. Unfortunately, the CKD population is characterized by many confounding factors in this context such as dietary restriction, increased age, increased transit time, intake of medication in general and antibiotics in specific, limited exercise, diabetes mellitus, etc. The focus of this Special Issue of Toxins will be on the gut-kidney axis in all its aspects: intestinal microbiome profiling, intestinally generated uremic toxins, confounding factors for a CKD population, possible interventions trying to decrease generation of toxins and this with the aim to decrease inflammation and to improve outcome of CKD patients.

Prof. Dr. Griet Glorieux
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Gut-kidney axis
  • Intestinal microbiota
  • Uremic toxins
  • Chronic kidney disease (CKD)
  • Confounders in CKD (old age, constipation, diabetes, medication (antibiotics), limited exercise,…)
  • Intestinal barrier
  • Characterization
  • Generation
  • Intervention (pre-, pro-, synbiotics)
  • Diet

Published Papers (4 papers)

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Research

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Open AccessArticle Distal Colon Motor Dysfunction in Mice with Chronic Kidney Disease: Putative Role of Uremic Toxins
Received: 16 April 2018 / Revised: 10 May 2018 / Accepted: 15 May 2018 / Published: 16 May 2018
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Abstract
Although gastrointestinal complications are a common feature of patients with chronic kidney disease (CKD), the impact of uremia on bowel motility remains poorly understood. The present study was, therefore, designed to investigate the impact of uremia on gut motility. Kidney failure was induced
[...] Read more.
Although gastrointestinal complications are a common feature of patients with chronic kidney disease (CKD), the impact of uremia on bowel motility remains poorly understood. The present study was, therefore, designed to investigate the impact of uremia on gut motility. Kidney failure was induced in mice by chemical nephrectomy using an adenine diet (0.25% w/w). Gastrointestinal transit time and colon motility were explored in vivo and ex vivo. Colons from control mice were incubated with uremic plasma or uremic toxins (urea, indoxyl-sulfate or p-cresyl-sulfate) at concentrations encountered in patients with end-stage renal disease. Mice fed an adenine diet for 3 weeks exhibited a 3-fold increase in plasma urea (p < 0.001) evidencing kidney failure. The median gastrointestinal transit time was doubled (1.8-fold, p < 0.001) while a reduction in colonic propulsive motility was observed in CKD mice (3-fold, p < 0.001). Colon from CKD mice exhibited an abnormal pattern of contraction associated with a blunted maximal force of contraction. Control colons incubated with plasma from hemodialysis patients exhibited a blunted level of maximal contraction (p < 0.01). Incubation with urea did not elicit any difference but incubation with indoxyl-sulfate or p-cresyl-sulfate decreased the maximal force of contraction (−66% and −55%, respectively. p < 0.01). Taken together, these data suggest that uremia impairs colon motility probably through the retention of uremic toxins. Colon dysmotility might contribute to the gastrointestinal symptoms often reported in patients with CKD. Full article
(This article belongs to the Special Issue The Intestine and Uremia)
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Review

Jump to: Research

Open AccessReview Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression
Received: 15 June 2018 / Revised: 13 July 2018 / Accepted: 17 July 2018 / Published: 19 July 2018
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Abstract
In chronic kidney disease (CKD), accumulation of uremic toxins is associated with an increased risk of CKD progression. Some uremic toxins result from nutrient processing by gut microbiota, yielding precursors of uremic toxins or uremic toxins themselves, such as trimethylamine N-Oxide (TMAO), p-cresyl
[...] Read more.
In chronic kidney disease (CKD), accumulation of uremic toxins is associated with an increased risk of CKD progression. Some uremic toxins result from nutrient processing by gut microbiota, yielding precursors of uremic toxins or uremic toxins themselves, such as trimethylamine N-Oxide (TMAO), p-cresyl sulphate, indoxyl sulphate and indole-3 acetic acid. Increased intake of some nutrients may modify the gut microbiota, increasing the number of bacteria that process them to yield uremic toxins. Circulating levels of nutrient-derived uremic toxins are associated to increased risk of CKD progression. This offers the opportunity for therapeutic intervention by either modifying the diet, modifying the microbiota, decreasing uremic toxin production by microbiota, increasing toxin excretion or targeting specific uremic toxins. We now review the link between nutrients, microbiota and uremic toxin with CKD progression. Specific focus will be placed on the generation specific uremic toxins with nephrotoxic potential, the decreased availability of bacteria-derived metabolites with nephroprotective potential, such as vitamin K and butyrate and the cellular and molecular mechanisms linking these toxins and protective factors to kidney diseases. This information provides a conceptual framework that allows the development of novel therapeutic approaches. Full article
(This article belongs to the Special Issue The Intestine and Uremia)
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Open AccessReview Intestinal Barrier Function in Chronic Kidney Disease
Received: 29 June 2018 / Revised: 16 July 2018 / Accepted: 18 July 2018 / Published: 19 July 2018
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Abstract
The kidneys are key contributors to body homeostasis, by virtue of controlled excretion of excessive fluid, electrolytes, and toxic waste products. The syndrome of uremia equals the altered physiology due to irreversible loss of kidney function that is left uncorrected for, despite therapeutic
[...] Read more.
The kidneys are key contributors to body homeostasis, by virtue of controlled excretion of excessive fluid, electrolytes, and toxic waste products. The syndrome of uremia equals the altered physiology due to irreversible loss of kidney function that is left uncorrected for, despite therapeutic intervention(s). The intestines and its microbial content are prime contributors to this syndrome. The intestinal barrier separates the self (or the so-called “milieu intérior”) from the environment. In the large intestine, the intestinal barrier keeps apart human physiology and the microbiota. The enterocytes and the extracellular mucin layer functions form a complex multilayered structure, facilitating complex bidirectional metabolic and immunological crosstalk. The current review focuses on the intestinal barrier in chronic kidney disease (CKD). Loss of kidney function results in structural and functional alterations of the intestinal barrier, contribution to the syndrome of uremia. Full article
(This article belongs to the Special Issue The Intestine and Uremia)
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Open AccessFeature PaperReview The Role of Gut Microbiota and Diet on Uremic Retention Solutes Production in the Context of Chronic Kidney Disease
Received: 26 March 2018 / Revised: 9 April 2018 / Accepted: 11 April 2018 / Published: 13 April 2018
Cited by 1 | PDF Full-text (671 KB) | HTML Full-text | XML Full-text
Abstract
Uremic retention solutes (URS) are associated with cardiovascular complications and poor survival in chronic kidney disease. The better understanding of the origin of a certain number of these toxins enabled the development of new strategies to reduce their production. URS can be classified
[...] Read more.
Uremic retention solutes (URS) are associated with cardiovascular complications and poor survival in chronic kidney disease. The better understanding of the origin of a certain number of these toxins enabled the development of new strategies to reduce their production. URS can be classified according to their origins (i.e., host, microbial, or exogenous). The discovery of the fundamental role that the intestinal microbiota plays in the production of many URS has reinstated nutrition at the heart of therapeutics to prevent the accumulation of URS and their deleterious effects. The intestinal microbiota is personalized and is strongly influenced by dietary habits, such as the quantity and the quality of dietary protein and fibers. Herein, this review out lines the role of intestinal microbiota on URS production and the recent discoveries on the effect of diet composition on the microbial balance in the host with a focus on the effect on URS production. Full article
(This article belongs to the Special Issue The Intestine and Uremia)
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