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Toxins
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Uremia and Metabolic Complications of Chronic Kidney Disease...
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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: closed (15 April 2020) | Viewed by 24612

Special Issue Editor

Prof. Christophe Soulage

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Guest Editor
University of Lyon, CarMeN lab, UMR INSERM U.1060 - INSA-Lyon, Villeurbanne, France
Special Issues, Collections and Topics in MDPI journals

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 submissions that pass pre-check are 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 2700 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

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Published Papers (4 papers)

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Research

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13 pages, 2223 KiB  
Article
Carbamoylated Nail Proteins as Assessed by Near-Infrared Analysis Are Associated with Load of Uremic Toxins and Mortality in Hemodialysis Patients
by Sander De Bruyne, Jonas Himpe, Sigurd E. Delanghe, Griet Glorieux, Wim Van Biesen, Marc L. De Buyzere, Marijn M. Speeckaert and Joris R. Delanghe
Toxins 2020, 12(2), 83; https://doi.org/10.3390/toxins12020083 - 26 Jan 2020
Cited by 5 | Viewed by 2644
Abstract
Carbamoylation is an important risk factor for accelerated atherogenesis and mortality in patients undergoing hemodialysis (HD). We intended to explore whether carbamoylation as assessed by near-infrared (NIR) analysis of nail proteins is associated with (a) plasma concentrations of representative uremic toxins and (b) [...] Read more.
Carbamoylation is an important risk factor for accelerated atherogenesis and mortality in patients undergoing hemodialysis (HD). We intended to explore whether carbamoylation as assessed by near-infrared (NIR) analysis of nail proteins is associated with (a) plasma concentrations of representative uremic toxins and (b) mortality in HD patients. A total of 53 healthy volunteers and 84 consecutive HD patients were enrolled in this cross-sectional cohort study. Standard laboratory methods were used to measure routine parameters, whereas levels of uremic toxins were determined using reversed-phase high-performance liquid chromatography (RP-HPLC). Spectra of distal fingernail clippings were obtained using an Avantes NIR spectrometer and processed using chemometric data analysis. The second derivative of the peak intensity at 1494 nm attributed to N-H amide bands from NH2 of carbamoyl (-CONH2) groups was higher in HD patients than in control subjects (p < 0.0001). Peak intensity levels were associated with age and plasma levels of representative uremic toxins. Cox-regression analysis revealed a significant association with all-cause mortality, even after adjustment for age. In conclusion, our data revealed that carbamoylation as assessed by NIR analysis of nail proteins is associated with plasma concentrations of uremic toxins and also with mortality in HD patients. Further research to explore whether it is a surrogate marker or a hard indicator of mortality risk is warranted. Full article
(This article belongs to the Special Issue Uremia and Metabolic Complications of Chronic Kidney Disease )
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11 pages, 304 KiB  
Article
Evaluation of Electrolyte Concentration and Pro-Inflammatory and Oxidative Status in Dogs with Advanced Chronic Kidney Disease under Dietary Treatment
by Doris Pereira Halfen, Douglas Segalla Caragelasco, Juliana Paschoalin de Souza Nogueira, Juliana Toloi Jeremias, Vivian Pedrinelli, Patrícia Massae Oba, Bruna Ruberti, Cristiana Fonseca Ferreira Pontieri, Marcia Mery Kogika and Marcio Antonio Brunetto
Toxins 2020, 12(1), 3; https://doi.org/10.3390/toxins12010003 - 19 Dec 2019
Cited by 6 | Viewed by 4074
Abstract
An integrated study on the effect of renal diet on mineral metabolism, fibroblast growth factor 23 (FGF-23), total antioxidant capacity, and inflammatory markers has not been performed previously. In this study, we evaluated the effects of renal diet on mineral metabolism, oxidative stress [...] Read more.
An integrated study on the effect of renal diet on mineral metabolism, fibroblast growth factor 23 (FGF-23), total antioxidant capacity, and inflammatory markers has not been performed previously. In this study, we evaluated the effects of renal diet on mineral metabolism, oxidative stress and inflammation in dogs with stage 3 or 4 of chronic kidney disease (CKD). Body condition score (BCS), muscle condition score (MCS), serum biochemical profile, ionized calcium (i-Ca), total calcium (t-Ca), phosphorus (P), urea, creatinine, parathyroid hormone (PTH), FGF-23, interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor alpha (TNF-α) and total antioxidant capacity (TAC) were measured at baseline (T0) and after 6 months of dietary treatment (T6). Serum urea, P, t-Ca, i-Ca, PTH, FGF-23, IL-6, IL-10, TNF-α and TAC measurements did not differ between T0 and T6. Serum creatinine (SCr) was increased at T6 and serum PTH concentrations were positively correlated with serum SCr and urea. i-Ca was negatively correlated with urea and serum phosphorus was positively correlated with FGF-23. Urea and creatinine were positively correlated. The combination of renal diet and support treatment over 6 months in dogs with CKD stage 3 or 4 was effective in controlling uremia, acid–base balance, blood pressure, total antioxidant capacity, and inflammatory cytokine levels and in maintaining BCS and MCS. Full article
(This article belongs to the Special Issue Uremia and Metabolic Complications of Chronic Kidney Disease )
10 pages, 2092 KiB  
Article
Proteomic Characterization of High-Density Lipoprotein Particles from Non-Diabetic Hemodialysis Patients
by Nans Florens, Catherine Calzada, Frédéric Delolme, Adeline Page, Fitsum Guebre Egziabher, Laurent Juillard and Christophe O. Soulage
Toxins 2019, 11(11), 671; https://doi.org/10.3390/toxins11110671 - 15 Nov 2019
Cited by 10 | Viewed by 2898
Abstract
Chronic kidney disease is associated with an increased cardiovascular risk, and altered biological properties of high-density lipoproteins (HDL) may play a role in these events. This study aimed to describe the HDL proteome from non-diabetic hemodialysis patients and identify potential pathways affected by [...] Read more.
Chronic kidney disease is associated with an increased cardiovascular risk, and altered biological properties of high-density lipoproteins (HDL) may play a role in these events. This study aimed to describe the HDL proteome from non-diabetic hemodialysis patients and identify potential pathways affected by the dysregulated expression of HDL proteins. HDL were sampled from nine non-diabetic hemodialysis (HD) and eight control patients. Samples were analyzed using a nano-RSLC coupled with a Q-Orbitrap. Data were processed by database searching using SequestHT against a human Swissprot database and quantified with a label-free quantification approach. Proteins that were in at least five of the eight control and six of the nine HD patients were analyzed. Analysis was based on pairwise ratios and the ANOVA hypothesis test. Among 522 potential proteins, 326 proteins were identified to be in the HDL proteome from HD and control patients, among which 10 were significantly upregulated and nine downregulated in HD patients compared to the control patients (p < 0.05). Up and downregulated proteins were involved in lipid metabolism, hemostasis, wound healing, oxidative stress, and apoptosis pathways. This difference in composition could partly explain HDL dysfunction in the chronic kidney disease (CKD) population and participate in the higher cardiovascular risk observed in this population. Full article
(This article belongs to the Special Issue Uremia and Metabolic Complications of Chronic Kidney Disease )
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Review

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23 pages, 1431 KiB  
Review
FGF23 and Phosphate–Cardiovascular Toxins in CKD
by Isabel Vogt, Dieter Haffner and Maren Leifheit-Nestler
Toxins 2019, 11(11), 647; https://doi.org/10.3390/toxins11110647 - 6 Nov 2019
Cited by 58 | Viewed by 14432
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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