Revised: May 21, 2013
Accepted: July 17, 2013
Published online: August 6, 2013
Processing time: 135 Days and 12 Hours
High prevalence of atherosclerosis and arterial calcification in chronic kidney disease is far beyond the explanation by common cardiovascular risk factors such as aging diabetes, hypertension and dyslipidemia. The magnitude of coronary artery calcification is independently and inversely associated with renal function. In addition to cardiovascular risk factors, other chronic kidney disease-related risks such as phosphate retention, excess of calcium and prolonged dialysis vintage also contribute to the development of vascular calcification. Strategies to lower vascular calcification burden in chronic kidney disease population should include minimizing chronic kidney disease and atherosclerotic risk factors. Current therapies available are non-calcium containing phosphate binders, low dose active vitamin D and calcimimetic agent. The role of bisphosphonates in vascular calcification in chronic kidney disease population remains unclear. Preliminary data on sodium thiosulfate are promising, however, larger studies on efficacy and patient outcomes are necessary. Several large randomized controlled trials have confirmed the lack of benefit of statin in attenuating the progression of vascular calcification.
Core tip: High prevalence of atherosclerosis and arterial calcification in chronic kidney disease is far beyond the explanation by common cardiovascular risk factors. Phosphate retention, excess of calcium and prolonged dialysis vintage also contribute to the development of vascular calcification. Current therapies available include non-calcium containing phosphate binders, low dose active vitamin D and calcimimetic agent. The role of bisphosphonates is unclear. Preliminary data on sodium thiosulfate are promising. Several randomized studies revealed the lack of benefit of statin in lowering vascular calcification.