Medial artery calcification in ESRD patients is associated with deposition of bone matrix proteins

Moe, Sharon M.; O’Neill, Kalisha D.; Duan, Danxia; Ahmed, Sadiq; Chen, Neal X.; Leapman, Stephen B.; Fineberg, Naomi S.; Kopecky, Kenyon K.

doi:10.1046/j.1523-1755.2002.00170.x

Cited by 404 publications

(327 citation statements)

References 30 publications

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“…In agreement with our findings, Moe et al have recently reported that, in patients with ESRD, positive immunostaining for OPN in the artery is stronger in diabetes than in non-diabetes [23]. Remarkably, the plasma OPN levels of two participants were above 1,000 ng/ml.…”

Section: Discussionsupporting

confidence: 93%

“…Several investigators have reported that the elevated expression of OPN in vasculature has a crucial role in atherosclerotic calcification [6,8,23,30]; however, the significance of whether the enhancement is inducible or preventive to the vascular calcification has not been fully revealed. In addition, recent studies have shown that, in vascular wall cells, the expression of OPN is accelerated by advanced glycation end-products [31] and mechanical stress [32].…”

Section: Discussionmentioning

confidence: 99%

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Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

et al. 2004

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Abstract. Osteopontin (OPN) is thought to play multiple roles in the progression of atherosclerotic plaque including diabetic vascular complications. However, it still remains unclear whether the level of OPN in vivo is indeed clinically associated with the progression of diabetic complications. This study evaluated whether the levels of OPN in plasma and urine are correlated with the progression of diabetic complications, such as retinopathy, neuropathy, and nephropathy in patients with type 2 diabetes. In 229 patients with type 2 diabetes, OPN level in plasma and urine was evaluated by both the severity of diabetic complications, such as retinopathy, neuropathy, and nephropathy, and the clinical characteristics and the substantial laboratory findings. Plasma OPN level increased significantly with aging and the progression of diabetic nephropathy, especially at the stage of renal failure (p<0.05). However, the level was not related to the progression of retinopathy or neuropathy, or to laboratory findings, such as HbA1c or serum lipids. In contrast, urinary OPN level was not associated with diabetic complications in any of the subjects. There was no correlation between the plasma and urinary values of OPN. The results established that the plasma OPN was elevated in proportion to the progression of diabetic nephropathy, indicating that the plasma concentration may be a potential diagnostic predictor of diabetic end-stage renal disease.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

et al. 2004

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“…Osteopontin levels were increased (25,26) and ␣ smooth muscle actin levels were decreased (25) in calcified medial layers of cutaneous blood vessels in patients with calcific uremic arteriolopathy. Furthermore, staining for osteopontin and other bone matrix molecules was strongly correlated with medial calcification in epigastric arteries of dialysis patients (27). These data support the concept that SMC undergo phenotypic conversion to osteogenic cell type in the presence of hyperphosphatemia in both animals and humans.…”

Section: Mechanistic Evidence For Hyperphosphatemiainduced Calcificationsupporting

confidence: 72%

Vascular Calcification

Giachelli

2003

Journal of the American Society of Nephrology

274

204

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Abstract. Uremic patients are prone to widespread ectopic extraskeletal calcification resulting from an imbalance of systemic inorganic phosphate (Pi). There can be serious consequences of this process, particularly when it results in the calcification of the vasculature. A recent study examined the response of cultured human aortic smooth muscle cells to varying levels of extracellular Pi. Cells that were exposed to Pi levels similar to those seen in uremic patients (Ͼ1.4 mmol/L) showed dose-dependent increases in cell culture calcium deposition. The results of this study also defined the role of elevated phosphate in transforming the vascular phenotype of these cells to an osteogenic phenotype, such that a predisposition for calcification was created. Pi-induced changes included increased expression of the osteogenic markers osteocalcin and core-binding factor-1 genes, the latter of which is considered a "master gene" critical for osteoblast differentiation. These changes occur early after exposure to high phosphate levels and seem to be mediated by a sodium-dependent phosphate co-transporter, Pit-1 (Glvr-1

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“…Concomitant with mineralization, the cells undergo a phenotypic change characterized by loss of smooth muscle specific gene expression and upregulation of genes commonly associated with bone differentiation including osteocalcin, osteopontin and Runx2. Similar phenotypic changes have also been observed in vivo in human as well as animal models of vascular calcification (46,49,50). Elevated P-induced phenotypic transition and mineralization were shown to be dependent on a sodium-dependent phosphate cotransporter, Pit-1, on the basis of their ability to be inhibited by phosphonoformic acid (37) and Pit-1 specific small interfering RNA (Giachelli and Li, unpublished data).…”

Section: Roles Of Ca and P In Vascular Smooth Muscle Cell Mineralizationsupporting

confidence: 54%

Vascular Calcification Mechanisms

Giachelli

2004

Journal of the American Society of Nephrology

492

400

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Medial artery calcification in ESRD patients is associated with deposition of bone matrix proteins

Cited by 404 publications

References 30 publications

Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

Vascular Calcification

Vascular Calcification Mechanisms

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