| Literature DB >> 31831119 |
Matthew Ray1, Anna Jovanovich2.
Abstract
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. Published by Elsevier Inc.Entities:
Keywords: Chronic kidney Disease mineral bone disorder; Hyperphosphatemia; Secondary hyperparathyroidism; Vascular calcification
Year: 2019 PMID: 31831119 DOI: 10.1053/j.ackd.2019.09.004
Source DB: PubMed Journal: Adv Chronic Kidney Dis ISSN: 1548-5595 Impact factor: 3.620