Publication: Phosphate and Cardiovascular Disease beyond Chronic Kidney Disease and Vascular Calcification
Issued Date
2018-01-01
Resource Type
ISSN
20902158
2090214X
2090214X
Other identifier(s)
2-s2.0-85046014585
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Mahidol University
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SCOPUS
Bibliographic Citation
International Journal of Nephrology. Vol.2018, (2018)
Suggested Citation
Sinee Disthabanchong Phosphate and Cardiovascular Disease beyond Chronic Kidney Disease and Vascular Calcification. International Journal of Nephrology. Vol.2018, (2018). doi:10.1155/2018/3162806 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/47077
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Title
Phosphate and Cardiovascular Disease beyond Chronic Kidney Disease and Vascular Calcification
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Abstract
© 2018 Sinee Disthabanchong. Phosphate is essential for life but its accumulation can be detrimental. In end-stage renal disease, widespread vascular calcification occurs as a result of chronic phosphate load. The accumulation of phosphate is likely to occur long before the rise in serum phosphate above the normal range since several observational studies in both general population and early-stage CKD patients have identified the relationship between high-normal serum phosphate and adverse cardiovascular outcomes. Consumption of food high in phosphate increases both fasting and postprandial serum phosphate and habitual intake of high phosphate diet is associated with aging, cardiac hypertrophy, endothelial dysfunction, and subclinical atherosclerosis. The decline in renal function and dietary phosphate load can increase circulating fibroblast growth factor-23 (FGF-23) which may have a direct impact on cardiomyocytes. Increased FGF-23 levels in both CKD and general populations are associated with left ventricular hypertrophy, congestive heart failure, atrial fibrillation, and mortality. Increased extracellular phosphate directly affects endothelial cells causing cell apoptosis and vascular smooth muscle cells (VSMCs) causing transformation to osteogenic phenotype. Excess of calcium and phosphate in the circulation can promote the formation of protein-mineral complex called calciprotein particles (CPPs). In CKD, these CPPs contain less calcification inhibitors, induce inflammation, and promote VSMC calcification.