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Special Issue "Uremia and Cardiovascular Disease"

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

Deadline for manuscript submissions: 30 April 2018

Special Issue Editor

Guest Editor
Prof. Dr. Ziad A. Massy

Division of Nephrology, Ambroise Paré Hospital, APHP, Paris-Ile-de-France-West Versailles-Saint-Quentin-en-Yvelines University (UVSQ), 9 avenue Charles de Gaulle, 92104 Boulogne Billancourt/Paris and Inserm U1018 Team5, CESP, UVSQ, University Paris Saclay, Villejuif, France
Website1 | Website2 | E-Mail
Interests: uremic toxins; cardiovascular; bone; cerebral disease

Special Issue Information

Dear Colleagues,

Chronic Kidney Disease (CKD) is common affecting 10–12% of the adult population, and 30% or more over 70 years of age. Cardiovascular disease (CVD) is the leading cause of death in CKD patients with a steadily increased risk as kidney function declines up to 10–20 times more in end-stage renal disease (ESRD) than in the general population. CKD is mainly associated with two types of CVD: Accelerated atherosclerosis and specific CKD-related CVD, including arteriosclerosis and cardiac abnormalities (i.e., left ventricular hypertrophy and diastolic dysfunction). CVD risk is associated with traditional risk factors (e.g., diabetes, hypertension, dyslipidemia, and smoking), and with additional CKD-related factors called uremic toxins. Uremic toxins are classified by molecular weight into three groups: Low-molecular-weight toxins (e.g., urea and phosphate), middle molecule toxins (e.g., Beta 2 mcroglobulin, fibroblast growth factor (FGF) 23), and protein-bound toxins (e.g., indoxyl sulfate and p-cresyl sulfate). Cardiovascular toxicity has been demonstrated extensively in in vitro, in vivo (animal) and clinical studies for several uremic toxins, such as phosphate, FGF23, indoxyl sulfate and p-cresyl sulfate. Uremic toxicity can alter different portions of the cardiovascular system, including the endothelium, cardiomyoctes, and cerebral vascular circulation.

CKD is associated with both extensive vascular calcification and abnormal bone remodelling. Vascular calcification has been recently recognized as an active cell-mediated process, similar to skeletal mineralization. Moreover, growing evidence points towards a close relationship between bone and vessel. What is the role of different uremic toxins in this cross-talk between bone and vessel? And how may contribute to the development of both vascular and bone remodelling derangements in CKD patients? These questions are currently under investigation.

The focus of this Special Issue of Toxins will be on the kidney–cardiovascular– bone axis, in all its aspects: Individual toxicity, organ toxicity, possible interventions trying to decrease generation of toxins and this with the aim to decrease CVD and to improve the outcome of CKD patients.

Prof. Dr. Ziad A. Massy
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 single-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.


  • uremic toxins
  • endothelium
  • smooth muscle cells
  • cardiomyocytes
  • cerebral circulation
  • bone
  • CKD

Published Papers (1 paper)

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Open AccessArticle Impact of the Oral Adsorbent AST-120 on Organ-Specific Accumulation of Uremic Toxins: LC-MS/MS and MS Imaging Techniques
Toxins 2018, 10(1), 19; doi:10.3390/toxins10010019
Received: 31 October 2017 / Revised: 14 December 2017 / Accepted: 26 December 2017 / Published: 28 December 2017
PDF Full-text (3054 KB) | HTML Full-text | XML Full-text | Supplementary Files
Elevated circulating uremic toxins are associated with a variety of symptoms and organ dysfunction observed in patients with chronic kidney disease (CKD). Indoxyl sulfate (IS) and p-cresyl sulfate (PCS) are representative uremic toxins that exert various harmful effects. We recently showed that
[...] Read more.
Elevated circulating uremic toxins are associated with a variety of symptoms and organ dysfunction observed in patients with chronic kidney disease (CKD). Indoxyl sulfate (IS) and p-cresyl sulfate (PCS) are representative uremic toxins that exert various harmful effects. We recently showed that IS induces metabolic alteration in skeletal muscle and causes sarcopenia in mice. However, whether organ-specific accumulation of IS and PCS is associated with tissue dysfunction is still unclear. We investigated the accumulation of IS and PCS using liquid chromatography/tandem mass spectrometry in various tissues from mice with adenine-induced CKD. IS and PCS accumulated in all 15 organs analyzed, including kidney, skeletal muscle, and brain. We also visualized the tissue accumulation of IS and PCS with immunohistochemistry and mass spectrometry imaging techniques. The oral adsorbent AST-120 prevented some tissue accumulation of IS and PCS. In skeletal muscle, reduced accumulation following AST-120 treatment resulted in the amelioration of renal failure-associated muscle atrophy. We conclude that uremic toxins can accumulate in various organs and that AST-120 may be useful in treating or preventing organ dysfunction in CKD, possibly by reducing tissue accumulation of uremic toxins. Full article
(This article belongs to the Special Issue Uremia and Cardiovascular Disease)

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