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Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification

DOI: 10.4061/2011/939613

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Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications. 1. Introduction Vascular calcification is a kind of extraosseous calcification and is associated with aging physiologically, and a number of disorders including ESRD, diabetes mellitus, and cardiovascular disease pathologically. Multifactorial processes contribute to VC in which derangements in calcium and phosphorus homeostasis plays an important role and becomes popular therapeutic target nowadays. In ESRD patients with vascular calcification, a mixture of intimal and medial calcification has been observed in the effected vessels with dominant medial involvement. The risk of CVD mortality in ESRD patients with vascular calcification is 20 to 30 times higher than that of the general population [1–5]. Although phosphate is important for diverse cellular and physiological functions, impaired renal function with resultant phosphate accumulation with consequent bone and mineral disorders and vascular calcification are major problems among nephrologists. The increased risk of CVD mortality by hyperphosphatemia was partially explained by the predisposition of this population to vascular calcification [6–8]. (Figure 1) Even in early stage CKD, serum phosphorus level disturbances are proved to promote vascular calcification, hypertension, myocardial hypertrophy, and heart failure [9–11]. Current understanding of relationship between phosphorus and those disorders becomes popular in medical field, with the hope of halting or retarding the vascular calcification from the very early status in those patients. Figure 1: Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO 4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals.

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