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Special Issue "The Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD)"

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

Deadline for manuscript submissions: 30 June 2019

Special Issue Editors

Guest Editor
Prof. Dr. Marc G. Vervloet

Department of Nephrology and Institute of Cardiovascular Research, VU University Medical Center, 1081 HV Amsterdam, The Netherlands
Website | E-Mail
Guest Editor
Prof. Dr. Mario Cozzolino

Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Milan, Italy
Website | E-Mail

Special Issue Information

Dear Colleagues,

For long times the field of CKD-MBD has been dominated by abnormalities in the concentrations of PTH, vitamin D, phosphate, FGF23 and calcium. Direct associations between these factors in isolation have been described, usually pointing to u-shaped associations with clinical endpoints. These observational data form base of current treatment guidelines.

Recently, rapidly expanding insights are changing the landscape of CKD-MBD. Novel insights point to more complex pathological mechanisms that connect classical biomarkers, in particular PTH and phosphate to clinical disease. Phosphate emerges as an integral component of a specific uremic milieu that drives vascular disease, suggesting that targeting phosphate toxicity is more than targeting hyperphosphatemia. In addition, the perspective on both PTH and bone is shifting from isolated factors to complex regulatory systems, which may culminate in different treatment paradigms for the future. In addition to changing views on classical biomarkers, more components appear to contribute to the syndrome of CKD-MBD. Among those are disturbed homeostasis of Magnesium, the role of macrophages in uremia-associated vascular disease, and recently discovered humoral systems like activin-activation in CKD

These exciting new aspects are all covered in this Special Issue of Toxins, entirely dedicated to the moving field of CKD-MBD. This issue is created in close collaboration with the ERA-EDTA working group on CKD-MBD and is Guest-Edited by Professors Mario Cozzolino and Professor Marc Vervloet.

Prof. Dr. Marc G. Vervloet
Prof. Dr. Mario Cozzolino
Guest Editors

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

  • CKD-MBD
  • Phosphate
  • PTH
  • Cardiovascular disease
  • Macrophages
  • Bone disease
  • Senescence

Published Papers (2 papers)

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Review

Open AccessReview
The Key Role of Phosphate on Vascular Calcification
Received: 20 February 2019 / Revised: 5 April 2019 / Accepted: 7 April 2019 / Published: 9 April 2019
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Abstract
Vascular calcification (VC) is common in dialysis and non-dialysis chronic kidney disease (CKD) patients, even in the early stage of the disease. For this reason, it can be considered a CKD hallmark. VC contributes to cardiovascular disease (CVD) and increased mortality among CKD [...] Read more.
Vascular calcification (VC) is common in dialysis and non-dialysis chronic kidney disease (CKD) patients, even in the early stage of the disease. For this reason, it can be considered a CKD hallmark. VC contributes to cardiovascular disease (CVD) and increased mortality among CKD patients, although it has not been proven. There are more than one type of VC and every form represents a marker of systemic vascular disease and is associated with a higher prevalence of CVD in CKD patients, as shown by several clinical studies. Major risk factors for VC in CKD include: Increasing age, dialysis vintage, hyperphosphatemia (particularly in the setting of intermittent or persistent hypercalcemia), and a positive net calcium and phosphate balance. Excessive oral calcium intake, including calcium-containing phosphate binders, increases the risk for VC. Moreover, it has been demonstrated that there is less VC progression with non-calcium-containing phosphate binders. Unfortunately, until now, a specific therapy to prevent progression or to facilitate regression of VC has been found, beyond careful attention to calcium and phosphate balance. Full article
(This article belongs to the Special Issue The Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD))
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Open AccessReview
Senescent Cells in Early Vascular Ageing and Bone Disease of Chronic Kidney Disease—A Novel Target for Treatment
Received: 31 December 2018 / Revised: 23 January 2019 / Accepted: 24 January 2019 / Published: 1 February 2019
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Abstract
Together with bone-mineral disorders, premature vascular ageing is a common feature of the uremic phenotype. A detailed understanding of mechanisms involved remains unclear and warrants further research. Available treatment options for end stage renal disease are principally dialysis and organ transplantation, as other [...] Read more.
Together with bone-mineral disorders, premature vascular ageing is a common feature of the uremic phenotype. A detailed understanding of mechanisms involved remains unclear and warrants further research. Available treatment options for end stage renal disease are principally dialysis and organ transplantation, as other treatment alternatives have proven insufficient. Chronic kidney disease (CKD) has been proposed as a model of early vascular and bone ageing, with accumulating evidence supporting the contribution of cellular senescence and the senescence-associated secretory phenotype (SASP) to cardiovascular pathology in CKD. Correspondingly, novel therapies based around the use of senolytic compounds and nuclear factor-erythroid-2-related factor 2 (Nrf2) agonists, have been suggested as attractive novel treatment options. In this review, we detail the contribution of the uremic environment to these processes underpinning ageing and how these relate to vascular health. Full article
(This article belongs to the Special Issue The Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD))
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