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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We appreciate the interest shown and comments made by Villa-Bellosta et al&#46; with respect to our recent publication&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">First&#44; we agree that the dialysis bath should be personalised to generally achieve neutral calcium balances&#46; As Gonz&#225;lez-Parra et al&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> effectively demonstrated in their article&#44; the predialysis plasma calcium cut-off points that would allow one or another concentration of calcium in the dialysis bath to be decided on seem to be around 0&#46;96<span class="elsevierStyleHsp" style=""></span>mmol&#47;l and 1&#46;01<span class="elsevierStyleHsp" style=""></span>mmol&#47;l &#40;8&#46;75&#8211;9&#46;15<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; respectively&#41;&#46; However&#44; the aim of our study was not to determine these cut-off points&#44; but to analyse changes in calcaemia with randomly assigned calcium baths&#44; and their relationship with phosphorus and bicarbonate&#44; in pursuit of a parallel with studies <span class="elsevierStyleItalic">in vitro</span> by Lomashvili et al&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> and De Solis et al&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> Hence patients were classified as hypo- or normocalcaemic based on 1&#46;16<span class="elsevierStyleHsp" style=""></span>mM&#44; the lower limit of normal determined by our laboratory&#46; When we analysed changes in calcaemia in our sample&#44; based on the bath used&#44; we observed that the 1&#46;25<span class="elsevierStyleHsp" style=""></span>mM calcium bath scarcely induced hypercalcaemia &#40;&#62;1&#46;3<span class="elsevierStyleHsp" style=""></span>mM&#41;&#44; while all patients dialysed with the 1&#46;5<span class="elsevierStyleHsp" style=""></span>mM bath completed the session with hypercalcaemia &#40;all independently of predialysis plasma calcium&#41;&#46; Therefore&#44; we understand that&#44; while the 1&#46;25<span class="elsevierStyleHsp" style=""></span>mM calcium bath could be considered to be &#8220;standard&#8221;&#44; some situations require higher or lower concentrations in order to achieve balances that are as neutral as possible&#44; as we initially remarked&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Second&#44; we have little to add to the comments made about the calcium-phosphorus product and the role historically attributed to it in vascular calcification&#46; As O&#8217;Neill said in his publication&#44; this entrenched dogma represents a simplistic interpretation with little scientific basis&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> since the key to this complex process lies in calcium more than phosphorus &#8212; to say nothing of the host of inductive and protective factors in vascular calcification proposed in recent years&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Finally&#44; the question of whether it is the induction of alkalaemia or the addition of bicarbonate that induces vascular calcification in the patient in haemodialysis is difficult to answer&#46; Indeed&#44; when bicarbonate is infused&#44; the increase in pH is lower than expected&#46; This may be explained on the one hand by the isohydric principle &#40;part of the bicarbonate is consumed thereby restoring other plasma buffers&#44; including phosphate&#44; thereby generating precursors of brushite and hydroxyapatite&#41;&#44; and on the other hand by respiratory compensation&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> The fact is that&#44; although the increase in pH following a dialysis session might seem unimportant and even transient&#44; this should not lead to underestimating the extent of underlying clinical-chemistry processes that are set in motion to buffer the alkalaemia induced in such a short space of time&#44; and that probably play a role in vascular calcification associated with haemodialysis&#46; In addition&#44; as Villa-Bellosta et al&#46; demonstrated in their article&#44; bicarbonate in itself is able to form hydroxyapatite crystals when combined with infused calcium&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">7</span></a> Based on the above-mentioned studies <span class="elsevierStyleItalic">in vitro</span>&#44;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">3&#44;4</span></a> it seems that the critical moment in which the addition of bicarbonate would become more harmful coincides with the first hour of a session&#44; when calcium increases in the presence of hyperphosphataemia&#46; Although translating results <span class="elsevierStyleItalic">in vitro</span> to daily clinical practice would be hasty and reductionist&#44; these finding should incite reflection on the potential alternatives&#46; Despite all this&#44; the use of bicarbonate has manifest benefits in bone and protein metabolism that in its day represented an advance with respect to acetate&#44; which is now obsolete&#46; This leads to considering other ways of administering bicarbonate&#44; for example by delaying its infusion during a session so that it does not coincide with the adverse clinical-chemistry scenario described above&#46; Research on new buffering compounds would undoubtedly yield another opinion to be considered&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In any case&#44; vascular calcification is extremely complex&#44; and it seems that various factors &#8212; active or passive&#44; within haemodialysis or outside of it &#8212; play one role or another in the process&#46;</p></span>"
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Letter to the Editor – Comments on published articles
Haemodialysis session: The perfect storm for vascular calcification
Sesión de hemodiálisis: la tormenta perfecta para la calcificación vascular
Miguel Seras, Ángel Luis Martín de Francisco
Corresponding author
Hospital Universitario Marqués de Valdecilla, Santander, Cantabria, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We appreciate the interest shown and comments made by Villa-Bellosta et al&#46; with respect to our recent publication&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">First&#44; we agree that the dialysis bath should be personalised to generally achieve neutral calcium balances&#46; As Gonz&#225;lez-Parra et al&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> effectively demonstrated in their article&#44; the predialysis plasma calcium cut-off points that would allow one or another concentration of calcium in the dialysis bath to be decided on seem to be around 0&#46;96<span class="elsevierStyleHsp" style=""></span>mmol&#47;l and 1&#46;01<span class="elsevierStyleHsp" style=""></span>mmol&#47;l &#40;8&#46;75&#8211;9&#46;15<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; respectively&#41;&#46; However&#44; the aim of our study was not to determine these cut-off points&#44; but to analyse changes in calcaemia with randomly assigned calcium baths&#44; and their relationship with phosphorus and bicarbonate&#44; in pursuit of a parallel with studies <span class="elsevierStyleItalic">in vitro</span> by Lomashvili et al&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> and De Solis et al&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> Hence patients were classified as hypo- or normocalcaemic based on 1&#46;16<span class="elsevierStyleHsp" style=""></span>mM&#44; the lower limit of normal determined by our laboratory&#46; When we analysed changes in calcaemia in our sample&#44; based on the bath used&#44; we observed that the 1&#46;25<span class="elsevierStyleHsp" style=""></span>mM calcium bath scarcely induced hypercalcaemia &#40;&#62;1&#46;3<span class="elsevierStyleHsp" style=""></span>mM&#41;&#44; while all patients dialysed with the 1&#46;5<span class="elsevierStyleHsp" style=""></span>mM bath completed the session with hypercalcaemia &#40;all independently of predialysis plasma calcium&#41;&#46; Therefore&#44; we understand that&#44; while the 1&#46;25<span class="elsevierStyleHsp" style=""></span>mM calcium bath could be considered to be &#8220;standard&#8221;&#44; some situations require higher or lower concentrations in order to achieve balances that are as neutral as possible&#44; as we initially remarked&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Second&#44; we have little to add to the comments made about the calcium-phosphorus product and the role historically attributed to it in vascular calcification&#46; As O&#8217;Neill said in his publication&#44; this entrenched dogma represents a simplistic interpretation with little scientific basis&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> since the key to this complex process lies in calcium more than phosphorus &#8212; to say nothing of the host of inductive and protective factors in vascular calcification proposed in recent years&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Finally&#44; the question of whether it is the induction of alkalaemia or the addition of bicarbonate that induces vascular calcification in the patient in haemodialysis is difficult to answer&#46; Indeed&#44; when bicarbonate is infused&#44; the increase in pH is lower than expected&#46; This may be explained on the one hand by the isohydric principle &#40;part of the bicarbonate is consumed thereby restoring other plasma buffers&#44; including phosphate&#44; thereby generating precursors of brushite and hydroxyapatite&#41;&#44; and on the other hand by respiratory compensation&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> The fact is that&#44; although the increase in pH following a dialysis session might seem unimportant and even transient&#44; this should not lead to underestimating the extent of underlying clinical-chemistry processes that are set in motion to buffer the alkalaemia induced in such a short space of time&#44; and that probably play a role in vascular calcification associated with haemodialysis&#46; In addition&#44; as Villa-Bellosta et al&#46; demonstrated in their article&#44; bicarbonate in itself is able to form hydroxyapatite crystals when combined with infused calcium&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">7</span></a> Based on the above-mentioned studies <span class="elsevierStyleItalic">in vitro</span>&#44;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">3&#44;4</span></a> it seems that the critical moment in which the addition of bicarbonate would become more harmful coincides with the first hour of a session&#44; when calcium increases in the presence of hyperphosphataemia&#46; Although translating results <span class="elsevierStyleItalic">in vitro</span> to daily clinical practice would be hasty and reductionist&#44; these finding should incite reflection on the potential alternatives&#46; Despite all this&#44; the use of bicarbonate has manifest benefits in bone and protein metabolism that in its day represented an advance with respect to acetate&#44; which is now obsolete&#46; This leads to considering other ways of administering bicarbonate&#44; for example by delaying its infusion during a session so that it does not coincide with the adverse clinical-chemistry scenario described above&#46; Research on new buffering compounds would undoubtedly yield another opinion to be considered&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In any case&#44; vascular calcification is extremely complex&#44; and it seems that various factors &#8212; active or passive&#44; within haemodialysis or outside of it &#8212; play one role or another in the process&#46;</p></span>"
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