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Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification.

Zheng CM, Lu KC, Wu CC, Hsu YH, Lin YF - Int J Nephrol (2011)

Bottom Line: Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients.Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification.Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology, Department of Medicine, Taipei Medical University-Shuang Ho Hospital, Taipei Medical University, Taipei 235, Taiwan.

ABSTRACT
Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications.

No MeSH data available.


Related in: MedlinePlus

Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals. Calcification inhibitors such as PPi inhibit hydroxyapatite precipitation, whereas fetuin-A, MGP, OPG, OPN, and BMP-7 antagonize calcification. VSMC: Vascular smooth muscle cells, Osf2/Cbfa1: Osteoblast-specific transcription factor, ROS: Reactive oxygen species, CaxP product: Calciumx phosphate produce, PO4(Pi): Phosphate, Pit-1: Sodium-phosphate cotransporter-1, ALP: Alkaline phosphatase, PPi: Pyrophosphate, MGP: Matrix Gla protein, OPG: Osteoprotegerin, OPN: Osteopontin, BMP: Bone morphogenic protein.
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Related In: Results  -  Collection


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fig1: Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals. Calcification inhibitors such as PPi inhibit hydroxyapatite precipitation, whereas fetuin-A, MGP, OPG, OPN, and BMP-7 antagonize calcification. VSMC: Vascular smooth muscle cells, Osf2/Cbfa1: Osteoblast-specific transcription factor, ROS: Reactive oxygen species, CaxP product: Calciumx phosphate produce, PO4(Pi): Phosphate, Pit-1: Sodium-phosphate cotransporter-1, ALP: Alkaline phosphatase, PPi: Pyrophosphate, MGP: Matrix Gla protein, OPG: Osteoprotegerin, OPN: Osteopontin, BMP: Bone morphogenic protein.

Mentions: Although phosphate is important for diverse cellular and physiological functions, impaired renal function with resultant phosphate accumulation with consequent bone and mineral disorders and vascular calcification are major problems among nephrologists. The increased risk of CVD mortality by hyperphosphatemia was partially explained by the predisposition of this population to vascular calcification [6–8]. (Figure 1) Even in early stage CKD, serum phosphorus level disturbances are proved to promote vascular calcification, hypertension, myocardial hypertrophy, and heart failure [9–11]. Current understanding of relationship between phosphorus and those disorders becomes popular in medical field, with the hope of halting or retarding the vascular calcification from the very early status in those patients.


Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification.

Zheng CM, Lu KC, Wu CC, Hsu YH, Lin YF - Int J Nephrol (2011)

Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals. Calcification inhibitors such as PPi inhibit hydroxyapatite precipitation, whereas fetuin-A, MGP, OPG, OPN, and BMP-7 antagonize calcification. VSMC: Vascular smooth muscle cells, Osf2/Cbfa1: Osteoblast-specific transcription factor, ROS: Reactive oxygen species, CaxP product: Calciumx phosphate produce, PO4(Pi): Phosphate, Pit-1: Sodium-phosphate cotransporter-1, ALP: Alkaline phosphatase, PPi: Pyrophosphate, MGP: Matrix Gla protein, OPG: Osteoprotegerin, OPN: Osteopontin, BMP: Bone morphogenic protein.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108197&req=5

fig1: Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals. Calcification inhibitors such as PPi inhibit hydroxyapatite precipitation, whereas fetuin-A, MGP, OPG, OPN, and BMP-7 antagonize calcification. VSMC: Vascular smooth muscle cells, Osf2/Cbfa1: Osteoblast-specific transcription factor, ROS: Reactive oxygen species, CaxP product: Calciumx phosphate produce, PO4(Pi): Phosphate, Pit-1: Sodium-phosphate cotransporter-1, ALP: Alkaline phosphatase, PPi: Pyrophosphate, MGP: Matrix Gla protein, OPG: Osteoprotegerin, OPN: Osteopontin, BMP: Bone morphogenic protein.
Mentions: Although phosphate is important for diverse cellular and physiological functions, impaired renal function with resultant phosphate accumulation with consequent bone and mineral disorders and vascular calcification are major problems among nephrologists. The increased risk of CVD mortality by hyperphosphatemia was partially explained by the predisposition of this population to vascular calcification [6–8]. (Figure 1) Even in early stage CKD, serum phosphorus level disturbances are proved to promote vascular calcification, hypertension, myocardial hypertrophy, and heart failure [9–11]. Current understanding of relationship between phosphorus and those disorders becomes popular in medical field, with the hope of halting or retarding the vascular calcification from the very early status in those patients.

Bottom Line: Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients.Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification.Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology, Department of Medicine, Taipei Medical University-Shuang Ho Hospital, Taipei Medical University, Taipei 235, Taiwan.

ABSTRACT
Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications.

No MeSH data available.


Related in: MedlinePlus