Mineral Bone Abnormalities and Vascular Calcifications

Vascular calcification (VC) is common in chronic kidney disease, increases in prevalence as patients progress to end-stage renal disease, and is significantly associated with mortality. VC is a complex and highly regulated process similar to bone formation whereby hydroxyapatite crystals deposit in the intimal or medial layer of arteries. Mineral bone abnormalities are common in chronic kidney disease; reduction in glomerular filtration rate and changes in vitamin D, parathyroid hormone, and fibroblast growth factor 23 result in the dysregulation of phosphorus and calcium metabolism. Cell culture studies, animal models, and observational and clinical studies all suggest this abnormal mineral metabolism plays a role in the initiation and progression of VC in kidney disease. This review will focus on these mineral bone abnormalities and how they may contribute to mechanisms that induce VC in kidney disease. Vascular calcification (VC) is common in chronic kidney disease, increases in prevalence as patients progress to end-stage renal disease, and is significantly associated with mortality. VC is a complex and highly regulated process similar to bone formation whereby hydroxyapatite crystals deposit in the intimal or medial layer of arteries. Mineral bone abnormalities are common in chronic kidney disease; reduction in glomerular filtration rate and changes in vitamin D, parathyroid hormone, and fibroblast growth factor 23 result in the dysregulation of phosphorus and calcium metabolism. Cell culture studies, animal models, and observational and clinical studies all suggest this abnormal mineral metabolism plays a role in the initiation and progression of VC in kidney disease. This review will focus on these mineral bone abnormalities and how they may contribute to mechanisms that induce VC in kidney disease.