
pmid: 17200044
Vascular calcification is highly prevalent and correlated with high rates of cardiovascular mortality in chronic kidney disease patients. Recent evidence suggests that mineral, hormonal, and metabolic imbalances that promote phenotype change in vascular cells as well as deficiencies in specific mineralization inhibitory pathways may be important contributory factors for vascular calcification in these patients. This article reviews current mechanisms proposed for the regulation of vascular calcification and data supporting their potential contribution to this process in chronic kidney disease.
Extracellular Matrix Proteins, Vitamin K, Bone Density Conservation Agents, alpha-2-HS-Glycoprotein, Calcium-Binding Proteins, Calcinosis, Blood Proteins, Antifibrinolytic Agents, Phosphates, Rats, Mice, Parathyroid Hormone, Bone Morphogenetic Proteins, Chronic Disease, Animals, Humans, Kidney Failure, Chronic, Kidney Diseases, Vascular Diseases, Vitamin D
Extracellular Matrix Proteins, Vitamin K, Bone Density Conservation Agents, alpha-2-HS-Glycoprotein, Calcium-Binding Proteins, Calcinosis, Blood Proteins, Antifibrinolytic Agents, Phosphates, Rats, Mice, Parathyroid Hormone, Bone Morphogenetic Proteins, Chronic Disease, Animals, Humans, Kidney Failure, Chronic, Kidney Diseases, Vascular Diseases, Vitamin D
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