الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Vascular disease (VD) is the leading cause of mortality and morbidity among patients with end stage renal disease (ESRD) who are on chronic regular dialysis. ( Gutierrez, et al 2013).
VD accounts for approximately 40% of mortality among patients on dialysis and is the main cause of hospitalization. Both traditional and non-traditional risk factors have been implicated in the development of VD in chronic dialysis patients. Traditional risk factors are those used to predict coronary heart disease outcomes in the general population and include hypertension, smoking, hyperlipidemia, hyperglycemia and obesity. Non-traditional risk factors (i.e., anemia, abnormal calcium/ phosphorus metabolism and malnutrition) are uremia-related factors that increase in prevalence as kidney function declines and contribute to the excess risk of VD observed in patients with chronic kidney disease (CKD). ( Lacquaniti, et al 2009).
Recent evidence suggests that the interaction of traditional and non traditional risk factors contribute to excessive and accelerated vascular calcification in ESRD patients. Intervention for those risk factors may delay the progression of vascular complications. (Van Bezooijen, et al 2008).
PTH is a component in a complex signaling system involving three structurally related ligands and two G protein-coupled receptors, which share significant amino acid sequence homology. PTH is a peptide hormone comprising 84 amino acids that is made by the parathyroid glands (and to a much smaller extend by the thymus) and acts through the PTH/PTH-related peptide (PTHrP) receptor to regulate the serum calcium concentration (Hoare SR et al., 2010).
Beginning in CKD stage 3, the ability of the kidneys to appropriately excrete a phosphate load is diminished, leading to hyperphosphatemia, elevated PTH (secondary hyperparathyrodism), and decreased 1,25(OH)2 vitamin D with associated elevations in the levels of FGF-23. The conversion of 25(OH) vitamin D to 1,25(OH)2 vitamin D is impaired, reducing intestinal calcium absorption and increasing PTH. (Y. Fang et al., 2014).