Bone and vascular metabolism: impact of chronic kidney disease

Abstract

The progression of chronic kidney disease (CKD) leads to a decrease in serum calcium levels and an increase in serum phosphorus levels. In order to maintain mineral homeostasis several regulatory mechanisms are triggered involving, among others, calcitriol, PTH and FGF23. In final stages of CKD these mechanisms become insufficient, leading to biochemical disorders, morphological bone changes and calcifications in vessels or other soft tissues which together are known as Chronic Kidney Disease and Mineral Bone Disorders (CKD-MBD). There are many studies that establish an association between vascular calcification and bone demineralization. Most of them indicate that the severity and progression of vascular calcifications are associated with bone mass and low bone turnover. The factors and signaling pathways involved in these processes are complex and are currently under investigation. Several factors have been identified as likely links of this association.
In this review we examine the parathyroid gland regulation with special emphasis on calcium-phosphorus-PTH-vitamin D-FGF23 axis in CKD and the association between vascular calcification and bone demineralization is discussed. As common factors have been involved in the pathogenesis of bone and vascular metabolism disorders, it has been suggested that common treatments may be use to correct these disorders.