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Matthew K. Williamson - One of the best experts on this subject based on the ideXlab platform.
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Artery Calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate
Kidney International, 2006Co-Authors: Paul A. Price, A M Roublick, Matthew K. WilliamsonAbstract:The present experiments investigate medial Artery Calcification in adult rats made uremic by feeding a synthetic diet containing 0.75% adenine for 4 weeks. Calcification was assessed by Alizarin red staining of intact aortas, by von Kossa staining of carotid Artery sections, and by calcium and phosphate incorporated into the thoracic aorta. The major conclusions are as follows: Lowering the protein content of the diet from 25 to 2.5% dramatically increases the frequency and extent of medial Artery Calcification in uremic rats without significantly affecting the elevation in serum creatinine, phosphate, or parathyroid hormone. This observation suggests that low dietary protein intake could be a risk factor for medial Artery Calcification in uremic patients. Medial Artery Calcification in uremic rats is prevented by a dose of ibandronate that inhibits bone resorption. The observation suggests that bone resorption inhibitors could prevent Artery Calcification in uremic patients. Medial Artery Calcification in uremic rats correlates with increased serum bone Gla protein (BGP; osteocalcin), but not with serum matrix Gla protein or fetuin. This finding indicates that it could be of interest to examine the relation between serum BGP and Artery Calcification in uremic patients. Each of these conclusions lends support for our hypothesis that medial Artery Calcification is linked to bone resorption. Future investigations of the as yet unknown biochemical basis for this link will be facilitated by the present discovery that a synthetic, 2.5% protein diet containing 0.75% adenine produces consistent and dramatic medial Calcification in adult rats within just 4 weeks.
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Serum levels of the fetuin-mineral complex correlate with Artery Calcification in the rat.
The Journal of biological chemistry, 2003Co-Authors: Paul A. Price, Matthew K. Williamson, Thao P. Nguyen, Truclinh N. ThanAbstract:The present studies were carried out to evaluate the possible association between the presence of the fetuin-mineral complex in serum and vitamin D-induced Artery Calcification. The first experiment shows that there is a fetuin-mineral complex in the blood of rats in which extensive Calcification of the Artery media has been induced by treatment with vitamin D for 96 h, and that there is no detectable fetuin-mineral complex in the blood of rats in which Artery Calcification has been inhibited by concurrent treatment with ibandronate or osteoprotegerin. The second experiment shows that the timing of vitamin D-induced Artery Calcification correlates with the timing of the maximal increase in serum fetuin-mineral complex levels. Whereas both results indicate that serum levels of the fetuin-mineral complex are indeed associated with vitamin D-induced Artery Calcification, the biochemical basis for this association is presently unclear. One possibility is that high levels of the fetuin-mineral complex cause defects in the ability of fetuin to prevent the growth of the mineral component, which then seeds Artery Calcification. Another possibility is that the fetuin-mineral complex is the downstream product of a pathway that begins with the true causative agent, and that the serum level of the fetuin-mineral complex is a marker for the activity of this agent in blood. An unexpected finding of the present studies is that vitamin D-induced Artery Calcification is also correlated with a 65 to 75% reduction in serum fetuin, a reduction that appears to be caused by the clearance of the fetuin-mineral complex from serum.
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bisphosphonates alendronate and ibandronate inhibit Artery Calcification at doses comparable to those that inhibit bone resorption
Arteriosclerosis Thrombosis and Vascular Biology, 2001Co-Authors: Paul A. Price, Samuel A. Faus, Matthew K. WilliamsonAbstract:Abstract—The present experiments were carried out to test the hypothesis that Artery Calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with the bisphosphonates alendronate and ibandronate will inhibit Artery Calcification. Artery Calcification was first induced by treatment of 42-day-old male rats with warfarin, a procedure that inhibits the γ-carboxylation of matrix Gla protein and has been shown to cause extensive Calcification of the Artery media within 2 weeks. These experiments revealed that ibandronate (0.05 mg · kg−1 · d−1) and alendronate (0.1 mg · kg−1 · d−1) completely inhibited Calcification of all arteries and heart valves examined after 2 and 4 weeks of warfarin treatment. A 10-fold lower dose of alendronate reduced Artery Calcification by 50% (P<0.005). These bisphosphonate doses are comparable to those that inhibit bone resorption in rats of this age. More rapid Artery Calcification was induced by treatment with warfarin together w...
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Bisphosphonates Alendronate and Ibandronate Inhibit Artery Calcification at Doses Comparable to Those That Inhibit Bone Resorption
Arteriosclerosis thrombosis and vascular biology, 2001Co-Authors: Paul A. Price, Samuel A. Faus, Matthew K. WilliamsonAbstract:Abstract—The present experiments were carried out to test the hypothesis that Artery Calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with the bisphosphonates alendronate and ibandronate will inhibit Artery Calcification. Artery Calcification was first induced by treatment of 42-day-old male rats with warfarin, a procedure that inhibits the γ-carboxylation of matrix Gla protein and has been shown to cause extensive Calcification of the Artery media within 2 weeks. These experiments revealed that ibandronate (0.05 mg · kg−1 · d−1) and alendronate (0.1 mg · kg−1 · d−1) completely inhibited Calcification of all arteries and heart valves examined after 2 and 4 weeks of warfarin treatment. A 10-fold lower dose of alendronate reduced Artery Calcification by 50% (P
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Warfarin-Induced Artery Calcification Is Accelerated by Growth and Vitamin D
Arteriosclerosis thrombosis and vascular biology, 2000Co-Authors: Paul A. Price, Samuel A. Faus, Matthew K. WilliamsonAbstract:The present studies demonstrate that growth and vitamin D treatment enhance the extent of Artery Calcification in rats given sufficient doses of Warfarin to inhibit gamma-carboxylation of matrix Gla protein, a Calcification inhibitor known to be expressed by smooth muscle cells and macrophages in the Artery wall. The first series of experiments examined the influence of age and growth status on Artery Calcification in Warfarin-treated rats. Treatment for 2 weeks with Warfarin caused massive focal Calcification of the Artery media in 20-day-old rats and less extensive focal Calcification in 42-day-old rats. In contrast, no Artery Calcification could be detected in 10-month-old adult rats even after 4 weeks of Warfarin treatment. To directly examine the importance of growth to Warfarin-induced Artery Calcification in animals of the same age, 20-day-old rats were fed for 2 weeks either an ad libitum diet or a 6-g/d restricted diet that maintains weight but prevents growth. Concurrent treatment of both dietary groups with Warfarin produced massive focal Calcification of the Artery media in the ad libitum-fed rats but no detectable Artery Calcification in the restricted-diet, growth-inhibited group. Although the explanation for the association between Artery Calcification and growth status cannot be determined from the present study, there was a relationship between higher serum phosphate and susceptibility to Artery Calcification, with 30% higher levels of serum phosphate in young, ad libitum-fed rats compared with either of the groups that was resistant to Warfarin-induced Artery Calcification, ie, the 10-month-old rats and the restricted-diet, growth-inhibited young rats. This observation suggests that increased susceptibility to Warfarin-induced Artery Calcification could be related to higher serum phosphate levels. The second set of experiments examined the possible synergy between vitamin D and Warfarin in Artery Calcification. High doses of vitamin D are known to cause Calcification of the Artery media in as little as 3 to 4 days. High doses of the vitamin K antagonist Warfarin are also known to cause Calcification of the Artery media, but at treatment times of 2 weeks or longer yet not at 1 week. In the current study, we investigated the synergy between these 2 treatments and found that concurrent Warfarin administration dramatically increased the extent of Calcification in the media of vitamin D-treated rats at 3 and 4 days. There was a close parallel between the effect of vitamin D dose on Artery Calcification and the effect of vitamin D dose on the elevation of serum calcium, which suggests that vitamin D may induce Artery Calcification through its effect on serum calcium. Because Warfarin treatment had no effect on the elevation in serum calcium produced by vitamin D, the synergy between Warfarin and vitamin D is probably best explained by the hypothesis that Warfarin inhibits the activity of matrix Gla protein as a Calcification inhibitor. High levels of matrix Gla protein are found at sites of Artery Calcification in rats treated with vitamin D plus Warfarin, and chemical analysis showed that the protein that accumulated was indeed not gamma-carboxylated. These observations indicate that although the gamma-carboxyglutamate residues of matrix Gla protein are apparently required for its function as a Calcification inhibitor, they are not required for its accumulation at Calcification sites.
Paul A. Price - One of the best experts on this subject based on the ideXlab platform.
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Artery Calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate
Kidney International, 2006Co-Authors: Paul A. Price, A M Roublick, Matthew K. WilliamsonAbstract:The present experiments investigate medial Artery Calcification in adult rats made uremic by feeding a synthetic diet containing 0.75% adenine for 4 weeks. Calcification was assessed by Alizarin red staining of intact aortas, by von Kossa staining of carotid Artery sections, and by calcium and phosphate incorporated into the thoracic aorta. The major conclusions are as follows: Lowering the protein content of the diet from 25 to 2.5% dramatically increases the frequency and extent of medial Artery Calcification in uremic rats without significantly affecting the elevation in serum creatinine, phosphate, or parathyroid hormone. This observation suggests that low dietary protein intake could be a risk factor for medial Artery Calcification in uremic patients. Medial Artery Calcification in uremic rats is prevented by a dose of ibandronate that inhibits bone resorption. The observation suggests that bone resorption inhibitors could prevent Artery Calcification in uremic patients. Medial Artery Calcification in uremic rats correlates with increased serum bone Gla protein (BGP; osteocalcin), but not with serum matrix Gla protein or fetuin. This finding indicates that it could be of interest to examine the relation between serum BGP and Artery Calcification in uremic patients. Each of these conclusions lends support for our hypothesis that medial Artery Calcification is linked to bone resorption. Future investigations of the as yet unknown biochemical basis for this link will be facilitated by the present discovery that a synthetic, 2.5% protein diet containing 0.75% adenine produces consistent and dramatic medial Calcification in adult rats within just 4 weeks.
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Serum levels of the fetuin-mineral complex correlate with Artery Calcification in the rat.
The Journal of biological chemistry, 2003Co-Authors: Paul A. Price, Matthew K. Williamson, Thao P. Nguyen, Truclinh N. ThanAbstract:The present studies were carried out to evaluate the possible association between the presence of the fetuin-mineral complex in serum and vitamin D-induced Artery Calcification. The first experiment shows that there is a fetuin-mineral complex in the blood of rats in which extensive Calcification of the Artery media has been induced by treatment with vitamin D for 96 h, and that there is no detectable fetuin-mineral complex in the blood of rats in which Artery Calcification has been inhibited by concurrent treatment with ibandronate or osteoprotegerin. The second experiment shows that the timing of vitamin D-induced Artery Calcification correlates with the timing of the maximal increase in serum fetuin-mineral complex levels. Whereas both results indicate that serum levels of the fetuin-mineral complex are indeed associated with vitamin D-induced Artery Calcification, the biochemical basis for this association is presently unclear. One possibility is that high levels of the fetuin-mineral complex cause defects in the ability of fetuin to prevent the growth of the mineral component, which then seeds Artery Calcification. Another possibility is that the fetuin-mineral complex is the downstream product of a pathway that begins with the true causative agent, and that the serum level of the fetuin-mineral complex is a marker for the activity of this agent in blood. An unexpected finding of the present studies is that vitamin D-induced Artery Calcification is also correlated with a 65 to 75% reduction in serum fetuin, a reduction that appears to be caused by the clearance of the fetuin-mineral complex from serum.
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bisphosphonates alendronate and ibandronate inhibit Artery Calcification at doses comparable to those that inhibit bone resorption
Arteriosclerosis Thrombosis and Vascular Biology, 2001Co-Authors: Paul A. Price, Samuel A. Faus, Matthew K. WilliamsonAbstract:Abstract—The present experiments were carried out to test the hypothesis that Artery Calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with the bisphosphonates alendronate and ibandronate will inhibit Artery Calcification. Artery Calcification was first induced by treatment of 42-day-old male rats with warfarin, a procedure that inhibits the γ-carboxylation of matrix Gla protein and has been shown to cause extensive Calcification of the Artery media within 2 weeks. These experiments revealed that ibandronate (0.05 mg · kg−1 · d−1) and alendronate (0.1 mg · kg−1 · d−1) completely inhibited Calcification of all arteries and heart valves examined after 2 and 4 weeks of warfarin treatment. A 10-fold lower dose of alendronate reduced Artery Calcification by 50% (P<0.005). These bisphosphonate doses are comparable to those that inhibit bone resorption in rats of this age. More rapid Artery Calcification was induced by treatment with warfarin together w...
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Bisphosphonates Alendronate and Ibandronate Inhibit Artery Calcification at Doses Comparable to Those That Inhibit Bone Resorption
Arteriosclerosis thrombosis and vascular biology, 2001Co-Authors: Paul A. Price, Samuel A. Faus, Matthew K. WilliamsonAbstract:Abstract—The present experiments were carried out to test the hypothesis that Artery Calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with the bisphosphonates alendronate and ibandronate will inhibit Artery Calcification. Artery Calcification was first induced by treatment of 42-day-old male rats with warfarin, a procedure that inhibits the γ-carboxylation of matrix Gla protein and has been shown to cause extensive Calcification of the Artery media within 2 weeks. These experiments revealed that ibandronate (0.05 mg · kg−1 · d−1) and alendronate (0.1 mg · kg−1 · d−1) completely inhibited Calcification of all arteries and heart valves examined after 2 and 4 weeks of warfarin treatment. A 10-fold lower dose of alendronate reduced Artery Calcification by 50% (P
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Warfarin-Induced Artery Calcification Is Accelerated by Growth and Vitamin D
Arteriosclerosis thrombosis and vascular biology, 2000Co-Authors: Paul A. Price, Samuel A. Faus, Matthew K. WilliamsonAbstract:The present studies demonstrate that growth and vitamin D treatment enhance the extent of Artery Calcification in rats given sufficient doses of Warfarin to inhibit gamma-carboxylation of matrix Gla protein, a Calcification inhibitor known to be expressed by smooth muscle cells and macrophages in the Artery wall. The first series of experiments examined the influence of age and growth status on Artery Calcification in Warfarin-treated rats. Treatment for 2 weeks with Warfarin caused massive focal Calcification of the Artery media in 20-day-old rats and less extensive focal Calcification in 42-day-old rats. In contrast, no Artery Calcification could be detected in 10-month-old adult rats even after 4 weeks of Warfarin treatment. To directly examine the importance of growth to Warfarin-induced Artery Calcification in animals of the same age, 20-day-old rats were fed for 2 weeks either an ad libitum diet or a 6-g/d restricted diet that maintains weight but prevents growth. Concurrent treatment of both dietary groups with Warfarin produced massive focal Calcification of the Artery media in the ad libitum-fed rats but no detectable Artery Calcification in the restricted-diet, growth-inhibited group. Although the explanation for the association between Artery Calcification and growth status cannot be determined from the present study, there was a relationship between higher serum phosphate and susceptibility to Artery Calcification, with 30% higher levels of serum phosphate in young, ad libitum-fed rats compared with either of the groups that was resistant to Warfarin-induced Artery Calcification, ie, the 10-month-old rats and the restricted-diet, growth-inhibited young rats. This observation suggests that increased susceptibility to Warfarin-induced Artery Calcification could be related to higher serum phosphate levels. The second set of experiments examined the possible synergy between vitamin D and Warfarin in Artery Calcification. High doses of vitamin D are known to cause Calcification of the Artery media in as little as 3 to 4 days. High doses of the vitamin K antagonist Warfarin are also known to cause Calcification of the Artery media, but at treatment times of 2 weeks or longer yet not at 1 week. In the current study, we investigated the synergy between these 2 treatments and found that concurrent Warfarin administration dramatically increased the extent of Calcification in the media of vitamin D-treated rats at 3 and 4 days. There was a close parallel between the effect of vitamin D dose on Artery Calcification and the effect of vitamin D dose on the elevation of serum calcium, which suggests that vitamin D may induce Artery Calcification through its effect on serum calcium. Because Warfarin treatment had no effect on the elevation in serum calcium produced by vitamin D, the synergy between Warfarin and vitamin D is probably best explained by the hypothesis that Warfarin inhibits the activity of matrix Gla protein as a Calcification inhibitor. High levels of matrix Gla protein are found at sites of Artery Calcification in rats treated with vitamin D plus Warfarin, and chemical analysis showed that the protein that accumulated was indeed not gamma-carboxylated. These observations indicate that although the gamma-carboxyglutamate residues of matrix Gla protein are apparently required for its function as a Calcification inhibitor, they are not required for its accumulation at Calcification sites.
Alaattin Yildiz - One of the best experts on this subject based on the ideXlab platform.
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Osteoprotegerin/RANKL Axis and Progression of Coronary Artery Calcification in Hemodialysis Patients
Clinical Journal of The American Society of Nephrology, 2012Co-Authors: Abdullah Ozkok, Yasar Caliskan, Tamer Sakaci, Gaye Erten, Gonca Emel Karahan, Alper Ozel, Abdulkadir Unsal, Alaattin YildizAbstract:BACKGROUND AND OBJECTIVES: Vascular Calcification is associated with increased cardiovascular mortality in chronic hemodialysis patients. This prospective study investigated the relationship between serum osteoprotegerin, receptor activator of NF-κB ligand, inflammatory markers, and progression of coronary Artery Calcification score. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Seventy-eight hemodialysis patients were enrolled. Serum IL-1β, IL-6, TNF-α, osteoprotegerin, receptor activator of NF-κB, fetuin A, and bone alkaline phosphatase were measured by ELISA. Coronary Artery Calcification score was measured two times with 1-year intervals, and patients were classified as progressive or nonprogressive. RESULTS: Baseline and first-year serum osteoprotegerin levels were significantly higher in the progressive than nonprogressive group (17.39±9.67 versus 12.90±6.59 pmol/L, P=0.02; 35.17±18.35 versus 24±11.65 pmol/L, P=0.002, respectively). The ratio of serum osteoprotegerin to receptor activator of NF-κB ligand at 1 year was significantly higher in the progressive group (0.26 [0.15-0.46] versus 0.18 [0.12-0.28], P=0.004). Serum osteoprotegerin levels were significantly correlated with coronary Artery Calcification score at both baseline (r=0.36, P=0.001) and 1 year (r=0.36, P=0.001). Importantly, progression in coronary Artery Calcification score significantly correlated with change in serum osteoprotegerin levels (r=0.39, P=0.001). In addition, serum receptor activator of NF-κB ligand levels were significantly inversely correlated with coronary Artery Calcification scores at both baseline (r=-0.29, P=0.01) and 1 year (r=-0.29, P=0.001). In linear regression analysis for predicting coronary Artery Calcification score progression, only baseline coronary Artery Calcification score and change in osteoprotegerin were retained as significant factors in the model. CONCLUSIONS: Baseline coronary Artery Calcification score and serum osteoprotegerin levels were significantly associated with progression of coronary Artery Calcification score in hemodialysis patients.
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Osteoprotegerin/RANKL Axis and Progression of Coronary Artery Calcification in Hemodialysis Patients
Clinical journal of the American Society of Nephrology : CJASN, 2012Co-Authors: Abdullah Ozkok, Yasar Caliskan, Tamer Sakaci, Gaye Erten, Gonca Emel Karahan, Alper Ozel, Abdulkadir Unsal, Alaattin YildizAbstract:Summary Background and objectives Vascular Calcification is associated with increased cardiovascular mortality in chronic hemodialysis patients. This prospective study investigated the relationship between serum osteoprotegerin, receptor activator of NF-kB ligand, inflammatory markers, and progression of coronary Artery Calcification score. Design, setting, participants, & measurements Seventy-eight hemodialysis patients were enrolled. Serum IL-1b, IL-6, TNF-a, osteoprotegerin, receptor activator of NF-kB, fetuin A, and bone alkaline phosphatase were measured by ELISA. Coronary Artery Calcification score was measured two times with 1-year intervals, and patients were classified as progressive or nonprogressive. Results Baseline and first-year serum osteoprotegerin levels were significantly higher in the progressive than nonprogressive group (17.3969.67 versus 12.9066.59 pmol/L, P=0.02; 35.17618.35 versus 24611.65 pmol/L, P=0.002, respectively). The ratio of serum osteoprotegerin to receptor activator of NF-kB ligand at 1 year was significantly higher in the progressive group (0.26 [0.15–0.46] versus 0.18 [0.12–0.28], P=0.004). Serum osteoprotegerin levels were significantly correlated with coronary Artery Calcification score at both baseline (r=0.36, P=0.001)and1year(r=0.36,P=0.001).Importantly,progressionincoronaryArteryCalcificationscoresignificantly correlatedwith changein serumosteoprotegerin levels (r=0.39,P=0.001). In addition, serumreceptor activator of NF-kB ligand levels were significantly inversely correlated with coronary Artery Calcification scores at both baseline (r=20.29, P=0.01) and 1 year (r=20.29, P=0.001). In linear regression analysis for predicting coronary Artery Calcification score progression, only baseline coronary Artery Calcification score and change in osteoprotegerin were retained as significant factors in the model. Conclusions Baseline coronary Artery Calcification score and serum osteoprotegerin levels were significantly associated with progression of coronary Artery Calcification score in hemodialysis patients. Clin J Am Soc Nephrol 7: 965–973, 2012. doi: 10.2215/CJN.11191111
Abdullah Ozkok - One of the best experts on this subject based on the ideXlab platform.
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Osteoprotegerin/RANKL Axis and Progression of Coronary Artery Calcification in Hemodialysis Patients
Clinical Journal of The American Society of Nephrology, 2012Co-Authors: Abdullah Ozkok, Yasar Caliskan, Tamer Sakaci, Gaye Erten, Gonca Emel Karahan, Alper Ozel, Abdulkadir Unsal, Alaattin YildizAbstract:BACKGROUND AND OBJECTIVES: Vascular Calcification is associated with increased cardiovascular mortality in chronic hemodialysis patients. This prospective study investigated the relationship between serum osteoprotegerin, receptor activator of NF-κB ligand, inflammatory markers, and progression of coronary Artery Calcification score. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Seventy-eight hemodialysis patients were enrolled. Serum IL-1β, IL-6, TNF-α, osteoprotegerin, receptor activator of NF-κB, fetuin A, and bone alkaline phosphatase were measured by ELISA. Coronary Artery Calcification score was measured two times with 1-year intervals, and patients were classified as progressive or nonprogressive. RESULTS: Baseline and first-year serum osteoprotegerin levels were significantly higher in the progressive than nonprogressive group (17.39±9.67 versus 12.90±6.59 pmol/L, P=0.02; 35.17±18.35 versus 24±11.65 pmol/L, P=0.002, respectively). The ratio of serum osteoprotegerin to receptor activator of NF-κB ligand at 1 year was significantly higher in the progressive group (0.26 [0.15-0.46] versus 0.18 [0.12-0.28], P=0.004). Serum osteoprotegerin levels were significantly correlated with coronary Artery Calcification score at both baseline (r=0.36, P=0.001) and 1 year (r=0.36, P=0.001). Importantly, progression in coronary Artery Calcification score significantly correlated with change in serum osteoprotegerin levels (r=0.39, P=0.001). In addition, serum receptor activator of NF-κB ligand levels were significantly inversely correlated with coronary Artery Calcification scores at both baseline (r=-0.29, P=0.01) and 1 year (r=-0.29, P=0.001). In linear regression analysis for predicting coronary Artery Calcification score progression, only baseline coronary Artery Calcification score and change in osteoprotegerin were retained as significant factors in the model. CONCLUSIONS: Baseline coronary Artery Calcification score and serum osteoprotegerin levels were significantly associated with progression of coronary Artery Calcification score in hemodialysis patients.
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Osteoprotegerin/RANKL Axis and Progression of Coronary Artery Calcification in Hemodialysis Patients
Clinical journal of the American Society of Nephrology : CJASN, 2012Co-Authors: Abdullah Ozkok, Yasar Caliskan, Tamer Sakaci, Gaye Erten, Gonca Emel Karahan, Alper Ozel, Abdulkadir Unsal, Alaattin YildizAbstract:Summary Background and objectives Vascular Calcification is associated with increased cardiovascular mortality in chronic hemodialysis patients. This prospective study investigated the relationship between serum osteoprotegerin, receptor activator of NF-kB ligand, inflammatory markers, and progression of coronary Artery Calcification score. Design, setting, participants, & measurements Seventy-eight hemodialysis patients were enrolled. Serum IL-1b, IL-6, TNF-a, osteoprotegerin, receptor activator of NF-kB, fetuin A, and bone alkaline phosphatase were measured by ELISA. Coronary Artery Calcification score was measured two times with 1-year intervals, and patients were classified as progressive or nonprogressive. Results Baseline and first-year serum osteoprotegerin levels were significantly higher in the progressive than nonprogressive group (17.3969.67 versus 12.9066.59 pmol/L, P=0.02; 35.17618.35 versus 24611.65 pmol/L, P=0.002, respectively). The ratio of serum osteoprotegerin to receptor activator of NF-kB ligand at 1 year was significantly higher in the progressive group (0.26 [0.15–0.46] versus 0.18 [0.12–0.28], P=0.004). Serum osteoprotegerin levels were significantly correlated with coronary Artery Calcification score at both baseline (r=0.36, P=0.001)and1year(r=0.36,P=0.001).Importantly,progressionincoronaryArteryCalcificationscoresignificantly correlatedwith changein serumosteoprotegerin levels (r=0.39,P=0.001). In addition, serumreceptor activator of NF-kB ligand levels were significantly inversely correlated with coronary Artery Calcification scores at both baseline (r=20.29, P=0.01) and 1 year (r=20.29, P=0.001). In linear regression analysis for predicting coronary Artery Calcification score progression, only baseline coronary Artery Calcification score and change in osteoprotegerin were retained as significant factors in the model. Conclusions Baseline coronary Artery Calcification score and serum osteoprotegerin levels were significantly associated with progression of coronary Artery Calcification score in hemodialysis patients. Clin J Am Soc Nephrol 7: 965–973, 2012. doi: 10.2215/CJN.11191111
Norman J. Beauchamp - One of the best experts on this subject based on the ideXlab platform.
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Cavernous carotid Artery Calcification and white matter ischemia.
AJNR. American journal of neuroradiology, 2003Co-Authors: Lukasz S. Babiarz, David M. Yousem, Bruce A. Wasserman, Warren B. Bilker, Norman J. BeauchampAbstract:BACKGROUND AND PURPOSE: The relevance of cavernous carotid Artery Calcification on unenhanced CT scans of the brain has recently been investigated against the backdrop of the widespread implementation of coronary Artery Calcification scoring. We sought to determine whether the degree of cavernous carotid Artery Calcification correlated with scores of white matter hyperintensity seen on MR images. In so doing, we sought to establish a relative risk for future stroke on the grade of carotid Calcification. METHODS: Neuroradiologic findings in 187 patients who underwent CT and MR imaging examinations within 1 month of each other were retrospectively reviewed. The degree of circumferential Calcification and thickness of Calcification were graded for the cavernous carotid arteries on the basis of CT findings. Using the scale developed by the Cardiovascular Health Study, the white matter was graded for degree of disease on the basis of MR findings. Correlation tests and regression analyses were performed to determine the impact of age, race, and sex on results. RESULTS: Although the cavernous carotid Calcification scores and the MR imaging white matter scores showed good correlation ( P CONCLUSION: After adjusting for age, cavernous carotid Calcification grades and MR imaging white matter scores do not show a significant correlation. The relative risk for future stroke cannot be predicted from cavernous carotid Calcifications.
