Mineral and bone disorder and vascular calcification in patients with chronic kidney disease

Abstract

Vascular calcifications has been associated with bone and mineral disorders. The alterations in the serum level of calcium concentrations and phosphate are importants factors implicated in the arterial calcification in chronic kidney disease. The pathogenesis of vascular calcification is a complex mechanism and not completely clear, being able to correspond to an active process of cellular transformation and heterotopic ossification. Beyond the hypercalcemia and hyperphosphatemia, they are involved in this process changes in the metabolism of inhibitors and promoters of calcification such as fetuin A, osteopontin, osteoprotegerin, and matrix gla protein. For the diagnosis of the calcified arterial injury are available several complementary methods, a method of estimate of the cardiovascular risk based on plain radiographs of the lumbar column and another method based on simple x-rays of the pelvis and hands. Below, we will present a review approching the link between vascular calcifications and mineral disorders.

Routine mammography: an opportunity for the diagnosis of chronic degenerative diseases? A cross-sectional study

“…In patients with CKD, medial layer calcification of the arteries appears to be associated with mineral and bone disorder, such as elevated serum levels of calcium and phosphate (41) . In patients with DM, we can find metabolic and inflammatory alterations (42,43) .…”

The Involvement of Notch1-RBP-Jk/Msx2 Signaling Pathway in Aortic Calcification of Diabetic Nephropathy Rats

“…The increase in serum calcium levels as well as calcium-phosphorus products can promote calcification. Hyperphosphatemia-related vascular calcification in patients with DN, end-stage renal disease, and metabolic syndrome occurs mainly in the arterial media [ 22 , 23 ]. Histological studies of model rats demonstrated deposition of calcium salts, which indicates successful establishment of a rat model of vascular calcification.…”

Serum sclerostin as a potential biomarker of vascular and valvular types of calcification in chronic kidney disease cases with and without maintenance hemodialysis

“…It is well established that the process of VC is controlled by a balance between pro-calcifying and anti-calcifying regulatory proteins acting locally in the vessel wall and/or systemically in the circulation [1,3]. The pathogenesis of VC in CKD results from an active process of transformation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells [1,4]. Radiological means for the detection of vascular and valvular types of calcification that associate CV complications remain the gold standard, yet several biomarkers are being studied among which sclerostin is a potential one.…”

“…Emerging experimental evidence suggests that some inhibitors of the canonical Wnt signaling pathway, which is actively involved in bone formation and VC, play a role linking VC and bone [3,4,6]. Vascular smooth muscles cells (VSMCs) undergo osteo/chondrogenic trans-differentiation in a pro-calcifying environment.…”

“…Vascular smooth muscles cells (VSMCs) undergo osteo/chondrogenic trans-differentiation in a pro-calcifying environment. The resulting osteoblast-like cells induce alkaline phosphatase (ALP) activity, responsible for the vascular tissue mineralization process [1,4]. Sclerostin is usually expressed in the late phase of VC, yet its role in the process of VC is still controversial.…”