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Vascular calcification and renal bone disorders.

Lu KC, Wu CC, Yen JF, Liu WC - ScientificWorldJournal (2014)

Bottom Line: Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality.These factors have roles in both promoting and inhibiting VC.In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology, Department of Medicine, Cardinal Tien Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 23148, Taiwan.

ABSTRACT
At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality. Many factors regulate the VC mechanism, which include imbalances in serum calcium and phosphate, systemic inflammation, RANK/RANKL/OPG triad, aldosterone, microRNAs, osteogenic transdifferentiation, and effects of vitamins. These factors have roles in both promoting and inhibiting VC. Patients with CKD usually have bone turnover problems. Patients with high bone turnover have increase of calcium and phosphate release from the bone. By contrast, when bone turnover is low, serum calcium and phosphate levels are frequently maintained at high levels because the reservoir functions of bone decrease. Both of these conditions will increase the possibility of VC. In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC. However, all of them may fight back the inhibition of bone formation resulting in fragile bone. There are several ways to treat VC depending on the bone turnover status of the individual. The main goals of therapy are to maintain normal bone turnover and protect against VC.

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Related in: MedlinePlus

Risk factors associated with medial arterial calcification (MAC) versus atherosclerosis in CKD (above). Simplified histopathology pictures of the MAC and atherosclerotic calcification (below). Disordered mineral metabolism in CKD with its associated characteristics of hyperphosphatemia, hypercalcemia, and renal osteodystrophy, as well as vitamin D perturbation and klotho deficiency, increases the risk for MAC. Oxidative stress and chronic inflammation in uremia also accelerate atherosclerosis. A number of risk factors can drive both pathologies. Both atherosclerotic calcification and medial calcification stiffen arterial conduit vessels, impairing heart function. The eccentric remodeling of atherosclerotic calcification also reduces lumen diameter and predisposes to acute thrombosis.
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fig2: Risk factors associated with medial arterial calcification (MAC) versus atherosclerosis in CKD (above). Simplified histopathology pictures of the MAC and atherosclerotic calcification (below). Disordered mineral metabolism in CKD with its associated characteristics of hyperphosphatemia, hypercalcemia, and renal osteodystrophy, as well as vitamin D perturbation and klotho deficiency, increases the risk for MAC. Oxidative stress and chronic inflammation in uremia also accelerate atherosclerosis. A number of risk factors can drive both pathologies. Both atherosclerotic calcification and medial calcification stiffen arterial conduit vessels, impairing heart function. The eccentric remodeling of atherosclerotic calcification also reduces lumen diameter and predisposes to acute thrombosis.

Mentions: Depending on the site, there are two main kinds of calcification: vascular wall calcification and cardiac valve calcification. Furthermore, VC can be divided into atherosclerosis and arteriosclerosis. This means it could be only one disease or two distinct ones existing at the same time. In CKD patients, most patients have two kinds of calcification simultaneously and overlapping pathological processes [7] (Figure 2).


Vascular calcification and renal bone disorders.

Lu KC, Wu CC, Yen JF, Liu WC - ScientificWorldJournal (2014)

Risk factors associated with medial arterial calcification (MAC) versus atherosclerosis in CKD (above). Simplified histopathology pictures of the MAC and atherosclerotic calcification (below). Disordered mineral metabolism in CKD with its associated characteristics of hyperphosphatemia, hypercalcemia, and renal osteodystrophy, as well as vitamin D perturbation and klotho deficiency, increases the risk for MAC. Oxidative stress and chronic inflammation in uremia also accelerate atherosclerosis. A number of risk factors can drive both pathologies. Both atherosclerotic calcification and medial calcification stiffen arterial conduit vessels, impairing heart function. The eccentric remodeling of atherosclerotic calcification also reduces lumen diameter and predisposes to acute thrombosis.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4127293&req=5

fig2: Risk factors associated with medial arterial calcification (MAC) versus atherosclerosis in CKD (above). Simplified histopathology pictures of the MAC and atherosclerotic calcification (below). Disordered mineral metabolism in CKD with its associated characteristics of hyperphosphatemia, hypercalcemia, and renal osteodystrophy, as well as vitamin D perturbation and klotho deficiency, increases the risk for MAC. Oxidative stress and chronic inflammation in uremia also accelerate atherosclerosis. A number of risk factors can drive both pathologies. Both atherosclerotic calcification and medial calcification stiffen arterial conduit vessels, impairing heart function. The eccentric remodeling of atherosclerotic calcification also reduces lumen diameter and predisposes to acute thrombosis.
Mentions: Depending on the site, there are two main kinds of calcification: vascular wall calcification and cardiac valve calcification. Furthermore, VC can be divided into atherosclerosis and arteriosclerosis. This means it could be only one disease or two distinct ones existing at the same time. In CKD patients, most patients have two kinds of calcification simultaneously and overlapping pathological processes [7] (Figure 2).

Bottom Line: Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality.These factors have roles in both promoting and inhibiting VC.In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology, Department of Medicine, Cardinal Tien Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 23148, Taiwan.

ABSTRACT
At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality. Many factors regulate the VC mechanism, which include imbalances in serum calcium and phosphate, systemic inflammation, RANK/RANKL/OPG triad, aldosterone, microRNAs, osteogenic transdifferentiation, and effects of vitamins. These factors have roles in both promoting and inhibiting VC. Patients with CKD usually have bone turnover problems. Patients with high bone turnover have increase of calcium and phosphate release from the bone. By contrast, when bone turnover is low, serum calcium and phosphate levels are frequently maintained at high levels because the reservoir functions of bone decrease. Both of these conditions will increase the possibility of VC. In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC. However, all of them may fight back the inhibition of bone formation resulting in fragile bone. There are several ways to treat VC depending on the bone turnover status of the individual. The main goals of therapy are to maintain normal bone turnover and protect against VC.

Show MeSH
Related in: MedlinePlus