Arterial Calcification in Chronic Kidney Disease: Whom? When? and How to Handle?
Journal: Journal of Urology & Nephrology (Vol.3, No. 1)Publication Date: 2016-12-30
Authors : Usama Abdel Azim Sharaf El Din; Mona Mansour Salem; Dina Ossama Abdulazim;
Page : 01-10
Keywords : Chronic kidney disease; CKD; Uremia; Vascular calcification; Arterial calcification; Cardiac calcification; Sevelamer; Calciphylaxis; Calcific uremic arteriolopathy; CUA; FGF23; Klotho;
Abstract
Chronic kidney disease (CKD) patients have the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the mortalities, with cardiovascular calcifications affecting the majority of those CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 (FGF23) and Klotho were incriminated in the pathogenesis of vascular calcification (VC) through different mechanisms including their effect on endothelium and arterial wall smooth muscle cells. In addition, deficient Klotho gene expression is a constant feature in CKD patients. This deficiency, not only promotes vascular pathology, but also has a role in the progression of the CKD. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, diagnostic tools, the ideal timing to prevent or to withhold the progression of VC and the different medications and medical procedures that can help to prolong the survival of CKD patients.
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Last modified: 2016-12-21 18:27:39