Special Issue "Uremia and Cardiovascular Disease"
Deadline for manuscript submissions: 30 April 2018
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
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Interests: uremic toxins; cardiovascular; bone; cerebral disease
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
Manuscript Submission Information
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- uremic toxins
- smooth muscle cells
- cerebral circulation