摘要
Cardiovascular disease is the leading cause of deathamong patients with chronic kidney disease （CKD）.Vascular calcification （VC） is one of the independentrisk factors associated with cardiovascular disease andcardiovascular mortality in both the general populationand CKD patients. Earlier evidence revealed substan-tially higher prevalence of VC in young adults on chron-ic hemodialysis compared to the general population inthe same age range, indicating the infuence of CKD-related risk factors on the development of VC. Patho-genesis of VC involves an active, highly organized cel-lular transformation of vascular smooth muscle cells tobone forming cells evidenced by the presence of bonematrix proteins in the calcifed arterial wall. VC occursin both the intima and the media of arterial wall withmedial calcification being more prevalent in CKD. Inaddition to traditional cardiovascular risks, risk factorsspecific to CKD such as phosphate retention, excessof calcium, history of dialysis, active vitamin D therapy in high doses and deficiency of calcification inhibitors play important roles in promoting the development of VC. Non-contrast multi-slice computed tomography has often been used to detect coronary artery calcif-cation. Simple plain radiographs of the lateral lumbar spine and pelvis can also detect VC in the abdominal aorta and femoral and iliac arteries. Currently, there is no specifc therapy to reverse VC. Reduction of calcium load, lowering phosphate retention using non-calcium containing phosphate binders, and moderate doses of active vitamin D may attenuate progression. Parenteral sodium thiosulfate has also been shown to delay VC progression.
Cardiovascular disease is the leading cause of death among patients with chronic kidney disease(CKD). Vascular calcification(VC) is one of the independent risk factors associated with cardiovascular disease and cardiovascular mortality in both the general population and CKD patients. Earlier evidence revealed substantially higher prevalence of VC in young adults on chronic hemodialysis compared to the general population in the same age range, indicating the influence of CKDrelated risk factors on the development of VC. Pathogenesis of VC involves an active, highly organized cellular transformation of vascular smooth muscle cells to bone forming cells evidenced by the presence of bone matrix proteins in the calcified arterial wall. VC occurs in both the intima and the media of arterial wall with medial calcification being more prevalent in CKD. In addition to traditional cardiovascular risks, risk factors specific to CKD such as phosphate retention, excess of calcium, history of dialysis, active vitamin D therapy in high doses and deficiency of calcification inhibitors play important roles in promoting the development of VC. Non-contrast multi-slice computed tomography has often been used to detect coronary artery calcifi-cation. Simple plain radiographs of the lateral lumbar spine and pelvis can also detect VC in the abdominal aorta and femoral and iliac arteries. Currently, there is no specific therapy to reverse VC. Reduction of calcium load, lowering phosphate retention using non-calcium containing phosphate binders, and moderate doses of active vitamin D may attenuate progression. Parenteral sodium thiosulfate has also been shown to delay VC progression.
基金
Supported by The Kidney Foundation of Thailand
