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AC develop in two distinct sites&#58; the intima and media layers of the large and medium-sized arterial wall<span class="elsevierStyleSup">10</span>&#46; <span class="elsevierStyleItalic">These two forms are frequently associated</span>&#46; Intima calcification occurs within atherosclerotic plaque and is a progressive feature of common atherosclerosis&#44; while media calcifications can occurs independently from atherosclerotic plaques and is frequently observed in medium sized arteries in CKD&#47;ESRD&#44; diabetes&#46; AC is tightly associated with aging and arterial remodeling&#44; including intima-media thickening&#44; but also changes of the geometry and function of aortic valves&#44; e&#46;g&#46;&#44; decreased aortic valve surface area and smaller valve opening<span class="elsevierStyleSup">11</span>&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">MECHANISMS OF ARTERIAL CALCIFICATION </span></p><p class="elsevierStylePara">The presence of dystrophic calcification in the arterial walls is a response to tissue injury&#44; represents a repair process&#44; and is a form of scar tissue<span class="elsevierStyleSup">12</span>&#46;&#160;Experimental and clinical studies have shown that AC is a process reflecting changes of the vascular smooth-muscle cells &#40;VSMC&#41; and pericytes from contractile to secretory phenotype&#41;&#46; VSMC synthesize bone-associated proteins&#44; including alkaline phosphatase&#44; osteocalcin&#44; osteopontin and a coat of collage-rich extracellular matrix&#44; and includes the formation of matrix vesicles&#44; nodules and apoptotic bodies&#44; which serve as initiation sites for apatite crystallization<span class="elsevierStyleSup">13&#44;14</span>&#46;&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">In vitro</span>&#44; VSMC differentiation towards osteoblast-like cells&#44; with subsequent mineralization&#44; is regulated by the balance between promoters and inhibitors of calcification&#44; and results from disruption of this balance in favor of promoters&#46; The secretory phenotype is initiated by the activation of Runx2 &#40;Cbfa1&#41; and osterix &#40;Osx&#41;&#44; transcrition factors that promote the differentiation of mesenchymal cells into the osteoblastic lineage<span class="elsevierStyleSup">15&#44;16</span>&#46; The Runx2 and Osx are activated upstream by several factors including Msx2&#44; Wnt and b-catenin signaling<span class="elsevierStyleSup">17</span>&#46; The stimuli initiating this &#8220;osteogenic cascade&#8221; include bone morphogenic proteins &#40;BMP 2&#44; 4&#41; and chronic injurious stimuli and metabolic toxicities including generation of reactive oxygen species &#40;ROS&#41;<span class="elsevierStyleSup">17-19</span>&#46; The result could be either VSMC apoptosis or stimulation of NFk-B and activation of inflammatory mediators TNFa&#44; IL-1&#44; IL-6&#44; and activation of macrophages<span class="elsevierStyleSup">19-23</span>&#46; Experimental studies using molecular imaging clearly showed that calcifications develops in parallel with inflammation in two phases&#58; early activation of macrophages and inflammation and calcification at later stage<span class="elsevierStyleSup">22</span> &#40;figure 1&#41;&#46;</p><p class="elsevierStylePara">Pooled uremic serum with high phophate concentration&#44; induced expression of Runx2<span class="elsevierStyleSup">24</span> and blocks the expression of genes responsibles for expression of contractile molecules<span class="elsevierStyleSup">13&#44;14</span>&#46; <span class="elsevierStyleSup">In vitro</span>&#44; the phosphate-stimulated calcification process can be inhibited by adding pyrophosphates that antagonize the cellular sodium-phosphate cotransport system &#40;PIT-1&#41;<span class="elsevierStyleSup">25</span>&#46; Recent study has shown tha phosphate induces the calcification process through a common pathway&#58; increasing mitochondrial ROS and activation of NFk-B pathway and transcription of osteogenic program with expression of Msx2-Wnt-Runx2<span class="elsevierStyleSup">26</span>&#46;</p><p class="elsevierStylePara">In the presence of normal serum&#44; VSMC do not calcified and can inhibit spontaneous calcium and phosphate precipitation in solution&#44; indicating that systemic calcification inhibitors such as fetuin-A are present in the serum<span class="elsevierStyleSup">27</span> and also in VSMCs who constitutively express potent local inhibitors of calcification&#44; such as matrix GLA protein<span class="elsevierStyleSup">28&#44;29</span>&#44; which may limit AC by binding to bone morphogenic proteins &#40;BMP-2&#41;<span class="elsevierStyleSup">29</span>&#46; Osteopontin and osteoprotegerin are potent inhibitors of AC in vivo&#44; and inactivation of their gene enhances the calcification process<span class="elsevierStyleSup">30&#44;31</span>&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CLINICAL IMPACT OF ARTERIAL CALCIFICATIONS </span></p><p class="elsevierStylePara">Intima calcification occurs in the context of common atherosclerosis&#44; progresses in parallel with the plaque evolution&#46; The arterial dysfunction result from narrowing of the arterial lumen with ischemia affecting the tissues and organs downstream&#46; The acute coronary events and infarction are more related to biomechanical stability of atherosclerotic plaques and the rupture of the plaque&#8217;s fibrous cap&#46; This results from mechanical discontinuity between the inclusion of rigid material &#40;calcium crystals&#41; into distensible material &#40;lipid core&#41; resulting in plaque vulnerability and rupture&#46; Although a higher coronary AC score is associated with a poorer cardiovascular prognosis&#44; the influence of calcification on plaque stability is controversial&#46; The results of several studies indicated that AC does not increase plaque vulnerability&#44; which seems more attributable to a large lipid pool&#44; thin fibrous cap and intensity of local inflammation<span class="elsevierStyleSup">32&#44;33</span>&#46;</p><p class="elsevierStylePara">Media calcification &#40;M&#246;nckeberg&#8217;s sclerosis or media calcinosis&#41; is characterized by diffuse mineral deposits within the arterial tunica media&#46; While media calcification is frequently observed with aging in the general population&#44; it is significantly more pronounced in patients with metabolic disorders&#44; such as metabolic syndrome&#44; diabetes or CKD&#46; Media calcification is concentric&#44; not extending into arterial lumen in its typical pure form and is associated with abnormal cushioning function of blood vessels &#40;arteriosclerosis-arterial hardening&#41; by promoting arterial stiffness<span class="elsevierStyleSup">34</span>&#46; The principal consequences of arterial stiffening are an abnormal arterial pressure wave &#40;characterized by increased systolic and decreased diastolic pressures&#44; resulting in high pulse pressure&#41; and increased aortic characteristic impedance&#44; a measure of the opposition of the aorta to oscillatory input &#40;i&#46;e&#46;&#44; stroke volume&#41;<span class="elsevierStyleSup">35</span>&#46; Because the two forms of AC are frequently associated the conduit and cushioning abnormalities could be associated&#46;<span class="elsevierStyleBold"> </span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">MANAGEMENT AND PREVENTION</span></p><p class="elsevierStylePara">AC rarely regress&#44; therefore&#44; the primary goals are prevention and stabilization of existing calcifications&#46; Because intimal AC are related to atherosclerosis&#44; the general approach is non-specific as advocated for patients with atherosclerosis&#58; control of blood lipids &#40;but no evidence of a benefit with statins&#41;&#44; use of aspirin&#44; treatment of obesity and hypertension&#44; physical activity&#44; smoking cessation&#44; and control of diabetes&#46; More specific preventive measures for patients with CKD or ESRD include controlling serum calcium and phosphate levels&#44; thereby avoiding oversuppression of parathyroid activity and ABD<span class="elsevierStyleSup">36</span>&#46; Disturbances in calcium and phosphate metabolism are associated with uremic bone disease&#44; and the results of several studies indicated that calcium overload is associated with AC development and progression&#44; suggesting that the overuse of high doses of calcium-based phosphate binders&#44; pharmacological doses of vitamin D&#44; and high calcium concentration in the dialysate should be avoided<span class="elsevierStyleSup">36-39</span>&#46; Those data suggest that the use of calcium-containing phosphate binders&#44; high intradialytic calcium load&#44; and overuse of active vitamin D should be avoided in elderly patients and in those who already have AC&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11175&#95;108&#95;21472&#95;en&#95;11175&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11175_108_21472_en_11175_f1.jpg" alt="Correlations between the abdominal aortic calcification score and high-sensitive C-RP&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Correlations between the abdominal aortic calcification score and high-sensitive C-RP&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">La calcificaci&#243;n arterial &#40;CA&#41; es una complicaci&#243;n com&#250;n en la enfermedad renal cr&#243;nica y la enfermedad renal en etapa terminal&#44; y cuyo alcance es diagn&#243;stico de una posterior mortalidad cardiovascular m&#225;s all&#225; de los factores de riesgo convencionales establecidos&#46; La CA se desarrolla en dos ubicaciones diferentes&#58; en las capas &#237;ntima y media de las paredes arteriales de gran y medio tama&#241;o&#46; Estas dos formas se encuentran frecuentemente asociadas&#46;<span class="elsevierStyleBold"> </span>La CA est&#225; estrechamente relacionada con el envejecimiento y el remodelado arterial&#44;<span class="elsevierStyleBold"> </span>que incluye el engrosamiento de la &#237;ntima-media<span class="elsevierStyleBold"> </span>y los cambios en la geometr&#237;a y la funci&#243;n de las v&#225;lvulas a&#243;rticas&#46; Se han recogido evidencias que se&#241;alan la naturaleza activa y regulada del proceso de calcificaci&#243;n&#46; Elevados niveles de fosfatos y calcio pueden estimular el cotransporte de fosfato dependiente del sodio que implique cambios osteobl&#225;sticos en la expresi&#243;n gen&#233;tica celular&#46; La CA es responsable del endurecimiento de las arterias&#44; con un aumento de la poscarga ventricular izquierda y perfusi&#243;n coronaria anormal como principales causas cl&#237;nicas&#46;</p>"
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Arterial calcification: cardiovascular function and clinical outcome
Gérard M. Londona, G.M.. Londonb
a INSERM U970, Paris and hopital F.H. Manhès, Fleury-Mérogis, Francia,
b INSERM U970, Paris and Hopital F.H. Manhès, Fleury-Mérogis, France,
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AC develop in two distinct sites&#58; the intima and media layers of the large and medium-sized arterial wall<span class="elsevierStyleSup">10</span>&#46; <span class="elsevierStyleItalic">These two forms are frequently associated</span>&#46; Intima calcification occurs within atherosclerotic plaque and is a progressive feature of common atherosclerosis&#44; while media calcifications can occurs independently from atherosclerotic plaques and is frequently observed in medium sized arteries in CKD&#47;ESRD&#44; diabetes&#46; AC is tightly associated with aging and arterial remodeling&#44; including intima-media thickening&#44; but also changes of the geometry and function of aortic valves&#44; e&#46;g&#46;&#44; decreased aortic valve surface area and smaller valve opening<span class="elsevierStyleSup">11</span>&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">MECHANISMS OF ARTERIAL CALCIFICATION </span></p><p class="elsevierStylePara">The presence of dystrophic calcification in the arterial walls is a response to tissue injury&#44; represents a repair process&#44; and is a form of scar tissue<span class="elsevierStyleSup">12</span>&#46;&#160;Experimental and clinical studies have shown that AC is a process reflecting changes of the vascular smooth-muscle cells &#40;VSMC&#41; and pericytes from contractile to secretory phenotype&#41;&#46; VSMC synthesize bone-associated proteins&#44; including alkaline phosphatase&#44; osteocalcin&#44; osteopontin and a coat of collage-rich extracellular matrix&#44; and includes the formation of matrix vesicles&#44; nodules and apoptotic bodies&#44; which serve as initiation sites for apatite crystallization<span class="elsevierStyleSup">13&#44;14</span>&#46;&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">In vitro</span>&#44; VSMC differentiation towards osteoblast-like cells&#44; with subsequent mineralization&#44; is regulated by the balance between promoters and inhibitors of calcification&#44; and results from disruption of this balance in favor of promoters&#46; The secretory phenotype is initiated by the activation of Runx2 &#40;Cbfa1&#41; and osterix &#40;Osx&#41;&#44; transcrition factors that promote the differentiation of mesenchymal cells into the osteoblastic lineage<span class="elsevierStyleSup">15&#44;16</span>&#46; The Runx2 and Osx are activated upstream by several factors including Msx2&#44; Wnt and b-catenin signaling<span class="elsevierStyleSup">17</span>&#46; The stimuli initiating this &#8220;osteogenic cascade&#8221; include bone morphogenic proteins &#40;BMP 2&#44; 4&#41; and chronic injurious stimuli and metabolic toxicities including generation of reactive oxygen species &#40;ROS&#41;<span class="elsevierStyleSup">17-19</span>&#46; The result could be either VSMC apoptosis or stimulation of NFk-B and activation of inflammatory mediators TNFa&#44; IL-1&#44; IL-6&#44; and activation of macrophages<span class="elsevierStyleSup">19-23</span>&#46; Experimental studies using molecular imaging clearly showed that calcifications develops in parallel with inflammation in two phases&#58; early activation of macrophages and inflammation and calcification at later stage<span class="elsevierStyleSup">22</span> &#40;figure 1&#41;&#46;</p><p class="elsevierStylePara">Pooled uremic serum with high phophate concentration&#44; induced expression of Runx2<span class="elsevierStyleSup">24</span> and blocks the expression of genes responsibles for expression of contractile molecules<span class="elsevierStyleSup">13&#44;14</span>&#46; <span class="elsevierStyleSup">In vitro</span>&#44; the phosphate-stimulated calcification process can be inhibited by adding pyrophosphates that antagonize the cellular sodium-phosphate cotransport system &#40;PIT-1&#41;<span class="elsevierStyleSup">25</span>&#46; Recent study has shown tha phosphate induces the calcification process through a common pathway&#58; increasing mitochondrial ROS and activation of NFk-B pathway and transcription of osteogenic program with expression of Msx2-Wnt-Runx2<span class="elsevierStyleSup">26</span>&#46;</p><p class="elsevierStylePara">In the presence of normal serum&#44; VSMC do not calcified and can inhibit spontaneous calcium and phosphate precipitation in solution&#44; indicating that systemic calcification inhibitors such as fetuin-A are present in the serum<span class="elsevierStyleSup">27</span> and also in VSMCs who constitutively express potent local inhibitors of calcification&#44; such as matrix GLA protein<span class="elsevierStyleSup">28&#44;29</span>&#44; which may limit AC by binding to bone morphogenic proteins &#40;BMP-2&#41;<span class="elsevierStyleSup">29</span>&#46; Osteopontin and osteoprotegerin are potent inhibitors of AC in vivo&#44; and inactivation of their gene enhances the calcification process<span class="elsevierStyleSup">30&#44;31</span>&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CLINICAL IMPACT OF ARTERIAL CALCIFICATIONS </span></p><p class="elsevierStylePara">Intima calcification occurs in the context of common atherosclerosis&#44; progresses in parallel with the plaque evolution&#46; The arterial dysfunction result from narrowing of the arterial lumen with ischemia affecting the tissues and organs downstream&#46; The acute coronary events and infarction are more related to biomechanical stability of atherosclerotic plaques and the rupture of the plaque&#8217;s fibrous cap&#46; This results from mechanical discontinuity between the inclusion of rigid material &#40;calcium crystals&#41; into distensible material &#40;lipid core&#41; resulting in plaque vulnerability and rupture&#46; Although a higher coronary AC score is associated with a poorer cardiovascular prognosis&#44; the influence of calcification on plaque stability is controversial&#46; The results of several studies indicated that AC does not increase plaque vulnerability&#44; which seems more attributable to a large lipid pool&#44; thin fibrous cap and intensity of local inflammation<span class="elsevierStyleSup">32&#44;33</span>&#46;</p><p class="elsevierStylePara">Media calcification &#40;M&#246;nckeberg&#8217;s sclerosis or media calcinosis&#41; is characterized by diffuse mineral deposits within the arterial tunica media&#46; While media calcification is frequently observed with aging in the general population&#44; it is significantly more pronounced in patients with metabolic disorders&#44; such as metabolic syndrome&#44; diabetes or CKD&#46; Media calcification is concentric&#44; not extending into arterial lumen in its typical pure form and is associated with abnormal cushioning function of blood vessels &#40;arteriosclerosis-arterial hardening&#41; by promoting arterial stiffness<span class="elsevierStyleSup">34</span>&#46; The principal consequences of arterial stiffening are an abnormal arterial pressure wave &#40;characterized by increased systolic and decreased diastolic pressures&#44; resulting in high pulse pressure&#41; and increased aortic characteristic impedance&#44; a measure of the opposition of the aorta to oscillatory input &#40;i&#46;e&#46;&#44; stroke volume&#41;<span class="elsevierStyleSup">35</span>&#46; Because the two forms of AC are frequently associated the conduit and cushioning abnormalities could be associated&#46;<span class="elsevierStyleBold"> </span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">MANAGEMENT AND PREVENTION</span></p><p class="elsevierStylePara">AC rarely regress&#44; therefore&#44; the primary goals are prevention and stabilization of existing calcifications&#46; Because intimal AC are related to atherosclerosis&#44; the general approach is non-specific as advocated for patients with atherosclerosis&#58; control of blood lipids &#40;but no evidence of a benefit with statins&#41;&#44; use of aspirin&#44; treatment of obesity and hypertension&#44; physical activity&#44; smoking cessation&#44; and control of diabetes&#46; More specific preventive measures for patients with CKD or ESRD include controlling serum calcium and phosphate levels&#44; thereby avoiding oversuppression of parathyroid activity and ABD<span class="elsevierStyleSup">36</span>&#46; Disturbances in calcium and phosphate metabolism are associated with uremic bone disease&#44; and the results of several studies indicated that calcium overload is associated with AC development and progression&#44; suggesting that the overuse of high doses of calcium-based phosphate binders&#44; pharmacological doses of vitamin D&#44; and high calcium concentration in the dialysate should be avoided<span class="elsevierStyleSup">36-39</span>&#46; Those data suggest that the use of calcium-containing phosphate binders&#44; high intradialytic calcium load&#44; and overuse of active vitamin D should be avoided in elderly patients and in those who already have AC&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11175&#95;108&#95;21472&#95;en&#95;11175&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11175_108_21472_en_11175_f1.jpg" alt="Correlations between the abdominal aortic calcification score and high-sensitive C-RP&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Correlations between the abdominal aortic calcification score and high-sensitive C-RP&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">La calcificaci&#243;n arterial &#40;CA&#41; es una complicaci&#243;n com&#250;n en la enfermedad renal cr&#243;nica y la enfermedad renal en etapa terminal&#44; y cuyo alcance es diagn&#243;stico de una posterior mortalidad cardiovascular m&#225;s all&#225; de los factores de riesgo convencionales establecidos&#46; La CA se desarrolla en dos ubicaciones diferentes&#58; en las capas &#237;ntima y media de las paredes arteriales de gran y medio tama&#241;o&#46; Estas dos formas se encuentran frecuentemente asociadas&#46;<span class="elsevierStyleBold"> </span>La CA est&#225; estrechamente relacionada con el envejecimiento y el remodelado arterial&#44;<span class="elsevierStyleBold"> </span>que incluye el engrosamiento de la &#237;ntima-media<span class="elsevierStyleBold"> </span>y los cambios en la geometr&#237;a y la funci&#243;n de las v&#225;lvulas a&#243;rticas&#46; Se han recogido evidencias que se&#241;alan la naturaleza activa y regulada del proceso de calcificaci&#243;n&#46; Elevados niveles de fosfatos y calcio pueden estimular el cotransporte de fosfato dependiente del sodio que implique cambios osteobl&#225;sticos en la expresi&#243;n gen&#233;tica celular&#46; La CA es responsable del endurecimiento de las arterias&#44; con un aumento de la poscarga ventricular izquierda y perfusi&#243;n coronaria anormal como principales causas cl&#237;nicas&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Arterial calcification &#40;AC&#41; is a common complication of CKD and ESRD&#44; and the extents of AC are predictive of subsequent cardiovascular mortality beyond established conventional risk factors&#46; AC develop in two distinct sites&#58; the intima and media layers of the large and medium-sized arterial wall&#46; These two forms are frequently associated&#46; AC is tightly associated with aging and arterial remodeling&#44; including intima-media thickening&#44; but also changes of the geometry and function of aortic valves&#46; Evidence has accumulated pointing to the active and regulated nature of the calcification process&#46; Elevated phosphate and calcium may stimulate sodium<span class="elsevierStyleBold">&#8211;</span>dependent phosphate cotransport involving osteoblast<span class="elsevierStyleBold">&#8211;</span>like changes in cellular gene expression&#46; AC is responsible for stiffening of the arteries with increased left ventricular afterload and abnormal coronary perfusion as the principal clinical consequences&#46;</p>"
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