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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

Bone turnover and vascular ossification in chronic kidney disease (CKD). Basically, bone cells have less vitality in patients with CKD than in normal persons. Thus, low bone turnover is part of the innate character of CKD. High PTH serum levels will overcome the indolent bone cells and lead to high turnover bone disease with the characteristics of relatively higher bone resorption than bone resorption. The high turnover status in SHPT can induce increased bone demineralization, which will increase calcium and inorganic phosphate release from bone into circulation. In contrast, overtreatment of CKD patients with Ca-salts, VDRA, or aluminum may cause them to develop low turnover bone disorders and low serum PTH levels. In patients with low bone turnover status, the decreased bone mineralization makes it difficult for calcium and inorganic phosphate to enter into bone, resulting in increased serum calcium and inorganic phosphate. Both high and low bone turnover disorders are characterized by a relatively higher degree of bone resorption than bone formation, which may contribute to the elevated serum calcium and inorganic phosphate levels, and aggravate vascular calcification/ossification.
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fig4: Bone turnover and vascular ossification in chronic kidney disease (CKD). Basically, bone cells have less vitality in patients with CKD than in normal persons. Thus, low bone turnover is part of the innate character of CKD. High PTH serum levels will overcome the indolent bone cells and lead to high turnover bone disease with the characteristics of relatively higher bone resorption than bone resorption. The high turnover status in SHPT can induce increased bone demineralization, which will increase calcium and inorganic phosphate release from bone into circulation. In contrast, overtreatment of CKD patients with Ca-salts, VDRA, or aluminum may cause them to develop low turnover bone disorders and low serum PTH levels. In patients with low bone turnover status, the decreased bone mineralization makes it difficult for calcium and inorganic phosphate to enter into bone, resulting in increased serum calcium and inorganic phosphate. Both high and low bone turnover disorders are characterized by a relatively higher degree of bone resorption than bone formation, which may contribute to the elevated serum calcium and inorganic phosphate levels, and aggravate vascular calcification/ossification.

Mentions: However, the relationship between low bone turnover and VC remains unclear [98]. Recent publications examining low or even high bone turnover discovered that VC is not influenced by bone turnover itself but is related to situations where bone resorption is greater than bone formation (Figure 4). These researchers found that VC can occur at any level of bone turnover [98]. As previously stated, serum phosphate may be one of the connections between bone turnover and VC. When bone turnover is low, as with adynamic bone, the amount of interchangeable calcium and phosphate is decreased, leading to higher concentrations associated with intake. Furthermore, bone resorption is more prominent than bone formation, interfering with the buffering function of the skeleton for extra phosphate. By contrast, when high bone turnover is present as in secondary hyperparathyroidism, a lot of phosphate is released from bone and, again, the reservoir function of the skeleton is destroyed [18]. Therefore, correcting the balance in bone, either high or low, will protect against the progression of VC [161].


Vascular calcification and renal bone disorders.

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

Bone turnover and vascular ossification in chronic kidney disease (CKD). Basically, bone cells have less vitality in patients with CKD than in normal persons. Thus, low bone turnover is part of the innate character of CKD. High PTH serum levels will overcome the indolent bone cells and lead to high turnover bone disease with the characteristics of relatively higher bone resorption than bone resorption. The high turnover status in SHPT can induce increased bone demineralization, which will increase calcium and inorganic phosphate release from bone into circulation. In contrast, overtreatment of CKD patients with Ca-salts, VDRA, or aluminum may cause them to develop low turnover bone disorders and low serum PTH levels. In patients with low bone turnover status, the decreased bone mineralization makes it difficult for calcium and inorganic phosphate to enter into bone, resulting in increased serum calcium and inorganic phosphate. Both high and low bone turnover disorders are characterized by a relatively higher degree of bone resorption than bone formation, which may contribute to the elevated serum calcium and inorganic phosphate levels, and aggravate vascular calcification/ossification.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Bone turnover and vascular ossification in chronic kidney disease (CKD). Basically, bone cells have less vitality in patients with CKD than in normal persons. Thus, low bone turnover is part of the innate character of CKD. High PTH serum levels will overcome the indolent bone cells and lead to high turnover bone disease with the characteristics of relatively higher bone resorption than bone resorption. The high turnover status in SHPT can induce increased bone demineralization, which will increase calcium and inorganic phosphate release from bone into circulation. In contrast, overtreatment of CKD patients with Ca-salts, VDRA, or aluminum may cause them to develop low turnover bone disorders and low serum PTH levels. In patients with low bone turnover status, the decreased bone mineralization makes it difficult for calcium and inorganic phosphate to enter into bone, resulting in increased serum calcium and inorganic phosphate. Both high and low bone turnover disorders are characterized by a relatively higher degree of bone resorption than bone formation, which may contribute to the elevated serum calcium and inorganic phosphate levels, and aggravate vascular calcification/ossification.
Mentions: However, the relationship between low bone turnover and VC remains unclear [98]. Recent publications examining low or even high bone turnover discovered that VC is not influenced by bone turnover itself but is related to situations where bone resorption is greater than bone formation (Figure 4). These researchers found that VC can occur at any level of bone turnover [98]. As previously stated, serum phosphate may be one of the connections between bone turnover and VC. When bone turnover is low, as with adynamic bone, the amount of interchangeable calcium and phosphate is decreased, leading to higher concentrations associated with intake. Furthermore, bone resorption is more prominent than bone formation, interfering with the buffering function of the skeleton for extra phosphate. By contrast, when high bone turnover is present as in secondary hyperparathyroidism, a lot of phosphate is released from bone and, again, the reservoir function of the skeleton is destroyed [18]. Therefore, correcting the balance in bone, either high or low, will protect against the progression of VC [161].

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