View clinical trials related to Vascular Calcification.
Filter by:Active vitamin D at therapeutic dose may prevent vascular calcification but in supraphysiologic dose may precipitate it.
Both Kidney transplantation (KT) and Chronic Kidney Disease (CKD) patients have reduced kidney function. Low serum magnesium is more prevalent in KT recipients. The present study examines the difference in vascular calcification between KT and CKD and its association with serum magnesium.
Chronic kidney disease (CKD) patients often have high levels of a substance called fibroblast growth factor-23 (FGF-23), a phosphorus excreting hormone, which has been related to heart disease. As kidney function declines, less phosphorus is removed by the kidneys and as a result phosphorus accumulates in the blood. In response to elevated phosphorus levels, more FGF-23 is released to help facilitate the excretion of extra phosphorus into the urine. In addition to effects on FGF-23, increased phosphorus levels can lead to calcification (hardening) of the blood vessels in the CKD population. Phosphate binding medicines are used in CKD patients to lower the amount of phosphorus absorbed by the stomach and intestines after eating meals and snacks. In patients with CKD, studies have shown that phosphate binders can lower FGF-23 levels in the blood. Lowering FGF-23 levels in CKD patients may also lower substances in the blood that cause calcification of blood vessels in the CKD population. This study is being done to determine if using phosphate binders, either sevelamer carbonate or calcium acetate, in the earlier stages kidney disease (before dialysis) can decrease FGF-23 and biomarkers (substances in the blood) associated with hardening of the blood vessels and heart disease.
The aim of this study was to evaluate whether successful sub-total parathyroidectomy retards cardiovascular calcification in patients with hemodialysis and to investigate the mechanism .
The aim of this cross-sectional study is to determine the correlation of coronary artery calcification as measured by electron-beam computerized tomography and coronary flow reserve measured by trans-thoracic Doppler echocardiography in hemodialysis patients. The investigators also assessed the carotid artery parameters by measuring intima media thickness that can accurately describe the process of arterial wall changes due to atherosclerosis. Possible association of coronary flow reserve with inflammation and arterial calcification in hemodialysis patients was also evaluated.
The purpose of this study is to determine if there is a link between calcium build up in the veins or arteries (including the veins/arteries of the heart) and deterioration of the bone. This will help understand if there is a connection between heart disease and bone disease.
The present study will examine the treatment effect of sodium thiosulfate on coronary calcification in patients on hemodialysis.
A not randomized , cross sectional study will be done to determine the possible association of coronary artery calcification (CAC) score assessed by multirow spiral computed tomography (MSCT) with specific and non specific uremic factor of vascular calcification.
Kidney disease is a fundamental part of medicine because of its prominence in Western society. Common conditions such as diabetes, hypertension and kidney infections can all progress to End-Stage Renal Disease (ESRD) also known as Stage 5 chronic kidney disease (CKD 5). Once ESRD has begun, kidney function is poor at best, thus the body is unable to effectively clear harmful toxins from the blood. A common feature of ESRD is vascular calcification, a process where blood vessels (especially arteries) attract deposits of the mineral calcium. Over time, these deposits harden and thicken in the layers of blood vessels, which limit blood flow to body tissues and can produce significant disease including hypertension, heart disease and stroke. Although the process of vascular calcification is unknown, there is mounting evidence that it is mediated by cellular events that are similar to those seen in bone formation with in the body (osteogenesis). With this point in mind, it has been suggested that agents medicine employs to limit excess bone formation will reduce the rate of vascular calcification in CKD Stage 5. This study will employ one group of drugs called bisphosphonates which have been used to limit bone formation. It will study their effect on vascular calcification in adult dialysis patients.
Cardiovascular disease is the major cause of death in the hemodialysis population and calcification of the major arteries (coronary, aorta, and carotid) are a play a central role in this process. The major causes of the calcification are many, including high levels of phosphorus, low levels of inhibitors of calcification, positive calcium balance, and oxidative stress. Once vascular calcification is present, it is usually progressive. There is no known treatment to reverse established vascular calcification. Sodium thiosulfate has been used extensively and safely to treat calcific uremic arteriopathy (a disease, in part due to calcification of small arteries) in dialysis patients. It increases the solubility of calcium by up to 100,000 fold and is also a potent anti-oxidant. It therefore has to potential to also decrease the amount of calcium in large arteries in dialysis patients and, hence improve survival. We will study hemodialysis (HD) patients at high risk for cardiovascular disease and death by obtaining a multidetector computerized tomography (MDCT) Scan of the coronary arteries, carotid arteries and aorta and an assessment of coronary artery stenoses by a simultaneous intravenous infusion of contrast. At the same setting, we will perform tests of pulse wave velocity (PWV) and carotid ultrasound carotid intima-media thickness(CIMT)studies. In those patients at high risk for cardiovascular death, defined as a coronary artery calcification score (CACS)of greater than 50, sodium thiosulfate at a dose of 12.5-25 gm/1.73 M2 will be infused over 15-30 minutes after each dialysis treatment for 5 months. The above studies will then be repeated.