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Abstract
Vascular calcification has now been recognized as a major problem in dialysis patients because of its strong influence on the prognosis. Along with the regulatory failure of calcification-inhibitory system, active phenotypic change of vascular smooth muscle cells (VSMCs) to osteoblast-like cells is also involved in the progression of vascular calcification.Delaying or improving the vascular calcification is thought to be very important to improve the cardiovascular mortality in dialysis patients. Several interventional trials against vascular calcification using non-calcium-containing phosphate binders, low-dose active vitamin D plus cinacalcet, modification of dialysate calcium concentration, and sodium thiosulfate have been done, and some trials including non-calcium-containing phosphate binders showed beneficial effect on delaying vascular calcification in dialysis patients. However, delaying or improving vascular calcification has not been clearly proved to result in improved cardiovascular event and/or mortality rate by prospective interventional randomized controlled trials in dialysis patients. Whether the improvement of vascular calcification could directly lead to the improvement of survival is an urgent issue of clinical trials in dialysis patients.
Highlights
As mentioned in a recent review [1], active atherosclerotic process has already begun in the early stages of chronic kidney disease (CKD), and atherosclerotic organ damages deteriorate along with the decreasing renal function
One of the most characteristic features of atherosclerosis seen in dialysis patients is vascular calcification, especially “medial calcification.”
Treatment with lanthanum carbonate was more effective compared to calcium carbonate in preventing the progression of CAC in patients on hemodialysis; regression by 6.4% was shown in the lanthanum-treated group vs. 41.2% progression in Vascular calcification might be merely one surrogate
Summary
As mentioned in a recent review [1], active atherosclerotic process has already begun in the early stages of chronic kidney disease (CKD), and atherosclerotic organ damages deteriorate along with the decreasing renal function. As to the relationship between coronary artery calcification score (CACS) and clinical outcomes, dialysis patients with higher CACS showed significantly higher rate of cardiovascular and all-cause mortality compared with those with mild or no CACS (Fig. 1) [7,8,9,10,11,12,13]. An early study by Shigematsu et al provided that the primary culture of radial artery VSMCs from a dialysis patient showed increased excretion of extracellular matrix with high affinity for calcium when incubated with a high phosphate medium (Pi = 5.4 mg/dl) [45].
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