Special Issue "Uremia and Metabolic Complications of Chronic Kidney Disease "

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

Deadline for manuscript submissions: 15 April 2020.

Special Issue Editor

Prof. Christophe Soulage
E-Mail
Guest Editor
University of Lyon, CarMeN lab, UMR INSERM U.1060 - INSA-Lyon, Villeurbanne, France

Special Issue Information

Dear colleagues,

Metabolic complications such as insulin resistance, dyslipidemia, or protein-energy wasting are now recognized as common features of patients with chronic kidney disease (CKD), although the underlying mechanisms still remain unclear. A growing body of evidence suggests that metabolic disorders are important contributors to the morbidity and mortality of these patients.

Renal clearance is impaired in patients with CKD, resulting in the accumulation of a large range of uremic solutes often referred to as uremic toxins if they exert deleterious biological activities. Several recent studies highlighted the role of the accumulation of these uremic toxins in the development of metabolic complications in CKD.

This Special Issue of Toxins will include original research articles and reviews on the role of the uremic milieu and uremic toxins in the pathogenesis of the metabolic complications of CKD. Generally speaking, this Special Issue will address all kinds of metabolic disturbances associated with uremia. These metabolic disturbances can non-exhaustively include anemia, insulin resistance, defects in insulin secretion, adipose tissue dysfunction, altered adipokine secretion, low-grade inflammation, and protein-energy wasting.

Prof. Christophe Soulage
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 1800 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

  • uremic toxin
  • uremia
  • insulin resistance
  • dyslipidemia
  • protein-energy wasting
  • metabolism
  • white adipose tissue

Published Papers (1 paper)

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Review

Open AccessReview
FGF23 and Phosphate–Cardiovascular Toxins in CKD
Toxins 2019, 11(11), 647; https://doi.org/10.3390/toxins11110647 - 06 Nov 2019
Abstract
Elevated levels of fibroblast growth factor 23 (FGF23) and phosphate are highly associated with increased cardiovascular disease and mortality in patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the secretion of the [...] Read more.
Elevated levels of fibroblast growth factor 23 (FGF23) and phosphate are highly associated with increased cardiovascular disease and mortality in patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the secretion of the phosphaturic hormone FGF23. In early stages of CKD, FGF23 prevents the increase of serum phosphate levels and thereby attenuates phosphate-induced vascular calcification, whereas in end-stage kidney disease, FGF23 fails to maintain phosphate homeostasis. Both hyperphosphatemia and elevated FGF23 levels promote the development of hypertension, vascular calcification, and left ventricular hypertrophy by distinct mechanisms. Therefore, FGF23 and phosphate are considered promising therapeutic targets to improve the cardiovascular outcome in CKD patients. Previous therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate, and consequently FGF23 levels. However, clinical trials proving the effects on the cardiovascular outcome are lacking. Recent publications provide evidence for new promising therapeutic interventions, such as magnesium supplementation and direct targeting of phosphate and FGF receptors to prevent toxicity of FGF23 and hyperphosphatemia in CKD patients. Full article
(This article belongs to the Special Issue Uremia and Metabolic Complications of Chronic Kidney Disease )
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