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Effect of Phosphorus on Valvular and Vascular Calcification in ESRD

2017-12-08 08:12:14 | BioPortfolio

Summary

Evaluation of the calcifying effect of phosphorus on vascular smooth muscle and detect the association between serum phosphorus and valvular and vascular calcification in end stage renal disease patients

Description

Cardiovascular disease (CVD) is the main cause of death in patients with end stage renal disease(ESRD). It is estimated that ESRD patients are 5 to 20 times more likely to die because of cardiovascular causes than the general population .

Traditional cardiovascular risk factors do not completely explain higher mortality rates among hemodialysis patients , and non traditional risk factors such as anemia, bone mineral disease, hyperhomocysteinemia, inflammation, hypercoagulability, and left ventricular hypertrophy (LVH) have been demonstrated to play an important role in this population.

A number of factors have been associated with progression of vascular calcification(VC) in dialysis patients. Associations with age and duration of dialysis , diabetes mellitus ,abnormalities of mineral metabolism as well as use and dose of calcium based phosphate binders have all been reported.

Hyperphosphatemia is a common problem among patients with ESRD. It is a highly prevalent condition, as almost 40% of the U.S. hemodialysis population has a serum phosphate( PO4) greater than 6.5 mg/dl . The overall mortality risk associated with serum phosphate( PO4) above 6.5 mg/dl was 27% greater than that of patients with PO4 levels between 2.4 and 6.5 mg/dl. It is speculated that elevate PO4 may aggravate the effects of coronary atherosclerosis through increased vascular calcification and smooth muscle proliferation . It has also been suggested that myocardial calcification, a consequence of elevated PO4, may alter microcirculatory hemodynamics through increased extravascular resistance and further compromise myocardial perfusion. We, therefore, hypothesized that the increased mortality risk associated with elevated PO4 levels was primarily related to cardiac rather than non-cardiac causes of death.

A number of non-invasive imaging techniques are now available to detect and quantify vascular calcification (VC). Indeed, plain x-rays of abdomen and extremities to identify macroscopic calcifications of aorta and peripheral arteries;echocardiography for assessment of valvular calcification;2D-ultrasound for calcification of carotid arteries, femoral arteries and aorta and computed tomography technologies constitute the current armamentarium for detection and quantification of cardiovascular calcification (VC) and its progression.

Electron beam computed tomography (EBCT) and multi-slice computed tomography (MSCT) represent the gold standard for assessing the extent of coronary artery and aorta calcification.MSCT is more widely available than EBCT

Study Design

Conditions

Vascular Calcification

Status

Not yet recruiting

Source

Assiut University

Results (where available)

View Results

Links

Published on BioPortfolio: 2017-12-08T08:12:14-0500

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Medical and Biotech [MESH] Definitions

Deposition of calcium into the blood vessel structures. Excessive calcification of the vessels are associated with ATHEROSCLEROTIC PLAQUES formation particularly after MYOCARDIAL INFARCTION (see MONCKEBERG MEDIAL CALCIFIC SCLEROSIS) and chronic kidney diseases which in turn increase VASCULAR STIFFNESS.

The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.

Secondary headache disorders attributed to a variety of cranial or cervical vascular disorders, such as BRAIN ISCHEMIA; INTRACRANIAL HEMORRHAGES; and CENTRAL NERVOUS SYSTEM VASCULAR MALFORMATIONS.

A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR C in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.

A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR D in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.

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