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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We read the article recently published in this journal by Seras et al&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> with particular interest&#44; and we would like to offer a few comments on it&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Regarding the variations in calcium concentration in the bath during dialysis&#44; we believe that&#44; effectively&#44; it should be personalised&#46; The main objective should be to create a calcium balance that is as neutral as possible during the session&#46; The reason is that a positive balance will result in a greater risk of vascular calcification&#44; and a negative balance will result in an increase in serum parathyroid hormone &#40;PTH&#41;&#46; To do this&#44; we believe that predialysis serum calcium is the best indicator of the concentrations in the dialysis bath&#46; It is not possible to extract from the intravascular space an amount of calcium equivalent to the amount physiologically eliminated through the urine in 48<span class="elsevierStyleHsp" style=""></span>h&#44; in a period of 4<span class="elsevierStyleHsp" style=""></span>h&#44; as that negative balance in such a short time increases PTH&#46; A recent publication by our group<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a> demonstrated that&#44; in patients with a predialysis ionised calcium concentration of 0&#46;96<span class="elsevierStyleHsp" style=""></span>mmol&#47;l or 8&#46;76<span class="elsevierStyleHsp" style=""></span>mg&#47;dl of total calcium&#44; the cut-off point for the calcium concentration in the bath is 1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#46; Below these values&#44; the patient creates a positive balance&#44; and above them&#44; the patient creates a negative balance&#46; With baths of 1&#46;5<span class="elsevierStyleHsp" style=""></span>mmol&#47;l of calcium above 9&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dl of predialysis total calcium &#40;Ca<span class="elsevierStyleSup">2&#43;</span> of 1&#46;01<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#41;&#44; a negative balance is created&#44; and below&#44; a positive balance is created&#46; In a study by Seras et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> the cut-off point was 1&#46;16<span class="elsevierStyleHsp" style=""></span>mmol&#47;l or 10&#46;4<span class="elsevierStyleHsp" style=""></span>mg&#47;dl total calcium &#40;estimating normal proteins of 7<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; This suggests that the group studied by the authors was very heterogeneous&#44; and that there were patients above and below the cut-off point of 0&#46;96 in both groups&#46; In our view&#44; the cut-off point of 1&#46;16<span class="elsevierStyleHsp" style=""></span>mmol&#47;l for ionised calcium is too high to establish it as a value to be used in one bath or another&#46; In addition&#44; we do not believe that using a bath of 1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;l is generally suitable in all patients to prevent vascular calcification&#44; as in patients with total calcium greater than 9&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dl &#40;Ca<span class="elsevierStyleSup">2&#43;</span> of 1&#46;01<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#41; it could induce a sustained increase in PTH&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Like Professor O&#8217;Neill&#39;s group&#44;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> we have demonstrated<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> that the product of Ca<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>Pi is not a determinant of vascular calcification&#46; In passive formation of calcium phosphate crystals in the vasculature&#44; the serum calcium concentration is more determinant than the serum phosphate concentration&#46; Moreover&#44; calcification may be induced with elevated calcium concentrations even when the phosphate concentration is low&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> Therefore&#44; even if phosphorus were to be eliminated during a dialysis session&#44; calcification could be induced in these patients provided that calcium is increased or maintained&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> However&#44; a few hours after completing the session&#44; phosphorus levels rise again&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Regarding the alkalinisation of the blood of patients during a dialysis session&#44; a distinction should be made between 2 matters&#46; An increase in serum pH is not the same as an increase in bicarbonate in the blood&#46; Blood pH is mostly governed by phosphate and bicarbonate&#44; and this influences vascular calcification given that alkalosis shifts the balance between the 2 types of phosphate in the blood &#40;H<span class="elsevierStyleInf">2</span>PO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#8722;</span> and HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">2&#8722;</span>&#41; towards the right&#46; This increases the concentration of HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">2&#8722;</span>&#44; which is a precursor of both brushite and hydroxyapatite&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> 2 crystals detected in calcifications&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">From a logical point of view&#44; to reduce acidosis in these patients&#44; adding bicarbonate to protocols was considered given its buffering capacity&#46; For example&#44; Seras et al&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> observed that after dialysis there was a loss of approximately 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl of phosphate&#44; an increase of approximately 5<span class="elsevierStyleHsp" style=""></span>mmol&#47;l of bicarbonate and a slight variation in blood pH &#40;0&#46;09 units&#41;&#46; The result was slight alkalinisation of the blood at the end of the dialysis session&#46; This modest change in blood pH suggested that this does not play a substantial role in vascular calcification&#46; This was especially likely to be the case as this slight alkalinisation of the blood was lost after several hours&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Finally&#44; without taking into account the fact that bicarbonate is responsible for the slight alkalinisation of the blood during dialysis&#44; bicarbonate also plays a determinant role in the production of calcium crystals&#44; including hydroxyapatite&#44; as one of our studies has shown&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Although it is a conceptual matter&#44; it should be known that bicarbonate is responsible for the increase in the calcification process&#44; whether directly by causing calcium crystals or indirectly by causing slight alkalinisation&#46; Therefore&#44; bicarbonate should be replaced with another buffering molecule or efforts should be made to reduce it during dialysis&#44; like calcium&#44; obviously within the available means&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">RVB is economically supported by a project &#40;SAF2014-60699-JIN&#41; of the Spanish Ministry of Economics and Competitiveness &#40;MINECO&#41; in association with ERDF funds&#46;</p></span></span>"
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Letter to the Editor – Comments on published articles
Comment to: Haemodialysis session: The perfect storm for vascular calcification
Comentario a: Sesión de hemodiálisis: la tormenta perfecta para la calcificación vascular
Ricardo Villa-Bellostaa,c,
Corresponding author
ricardo.villa@fjd.es

Corresponding author.
, Jesús Egidoa,b,c, Emilio González-Parrab
a Instituto de Investigación Sanitaria, Fundación Jiménez Díaz (IIS-FJD), Madrid, Spain
b Servicio de Nefrología, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Madrid, Spain
c Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We read the article recently published in this journal by Seras et al&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> with particular interest&#44; and we would like to offer a few comments on it&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Regarding the variations in calcium concentration in the bath during dialysis&#44; we believe that&#44; effectively&#44; it should be personalised&#46; The main objective should be to create a calcium balance that is as neutral as possible during the session&#46; The reason is that a positive balance will result in a greater risk of vascular calcification&#44; and a negative balance will result in an increase in serum parathyroid hormone &#40;PTH&#41;&#46; To do this&#44; we believe that predialysis serum calcium is the best indicator of the concentrations in the dialysis bath&#46; It is not possible to extract from the intravascular space an amount of calcium equivalent to the amount physiologically eliminated through the urine in 48<span class="elsevierStyleHsp" style=""></span>h&#44; in a period of 4<span class="elsevierStyleHsp" style=""></span>h&#44; as that negative balance in such a short time increases PTH&#46; A recent publication by our group<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a> demonstrated that&#44; in patients with a predialysis ionised calcium concentration of 0&#46;96<span class="elsevierStyleHsp" style=""></span>mmol&#47;l or 8&#46;76<span class="elsevierStyleHsp" style=""></span>mg&#47;dl of total calcium&#44; the cut-off point for the calcium concentration in the bath is 1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#46; Below these values&#44; the patient creates a positive balance&#44; and above them&#44; the patient creates a negative balance&#46; With baths of 1&#46;5<span class="elsevierStyleHsp" style=""></span>mmol&#47;l of calcium above 9&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dl of predialysis total calcium &#40;Ca<span class="elsevierStyleSup">2&#43;</span> of 1&#46;01<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#41;&#44; a negative balance is created&#44; and below&#44; a positive balance is created&#46; In a study by Seras et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> the cut-off point was 1&#46;16<span class="elsevierStyleHsp" style=""></span>mmol&#47;l or 10&#46;4<span class="elsevierStyleHsp" style=""></span>mg&#47;dl total calcium &#40;estimating normal proteins of 7<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; This suggests that the group studied by the authors was very heterogeneous&#44; and that there were patients above and below the cut-off point of 0&#46;96 in both groups&#46; In our view&#44; the cut-off point of 1&#46;16<span class="elsevierStyleHsp" style=""></span>mmol&#47;l for ionised calcium is too high to establish it as a value to be used in one bath or another&#46; In addition&#44; we do not believe that using a bath of 1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;l is generally suitable in all patients to prevent vascular calcification&#44; as in patients with total calcium greater than 9&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dl &#40;Ca<span class="elsevierStyleSup">2&#43;</span> of 1&#46;01<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#41; it could induce a sustained increase in PTH&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Like Professor O&#8217;Neill&#39;s group&#44;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> we have demonstrated<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> that the product of Ca<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>Pi is not a determinant of vascular calcification&#46; In passive formation of calcium phosphate crystals in the vasculature&#44; the serum calcium concentration is more determinant than the serum phosphate concentration&#46; Moreover&#44; calcification may be induced with elevated calcium concentrations even when the phosphate concentration is low&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> Therefore&#44; even if phosphorus were to be eliminated during a dialysis session&#44; calcification could be induced in these patients provided that calcium is increased or maintained&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> However&#44; a few hours after completing the session&#44; phosphorus levels rise again&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Regarding the alkalinisation of the blood of patients during a dialysis session&#44; a distinction should be made between 2 matters&#46; An increase in serum pH is not the same as an increase in bicarbonate in the blood&#46; Blood pH is mostly governed by phosphate and bicarbonate&#44; and this influences vascular calcification given that alkalosis shifts the balance between the 2 types of phosphate in the blood &#40;H<span class="elsevierStyleInf">2</span>PO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#8722;</span> and HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">2&#8722;</span>&#41; towards the right&#46; This increases the concentration of HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">2&#8722;</span>&#44; which is a precursor of both brushite and hydroxyapatite&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> 2 crystals detected in calcifications&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">From a logical point of view&#44; to reduce acidosis in these patients&#44; adding bicarbonate to protocols was considered given its buffering capacity&#46; For example&#44; Seras et al&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> observed that after dialysis there was a loss of approximately 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl of phosphate&#44; an increase of approximately 5<span class="elsevierStyleHsp" style=""></span>mmol&#47;l of bicarbonate and a slight variation in blood pH &#40;0&#46;09 units&#41;&#46; The result was slight alkalinisation of the blood at the end of the dialysis session&#46; This modest change in blood pH suggested that this does not play a substantial role in vascular calcification&#46; This was especially likely to be the case as this slight alkalinisation of the blood was lost after several hours&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Finally&#44; without taking into account the fact that bicarbonate is responsible for the slight alkalinisation of the blood during dialysis&#44; bicarbonate also plays a determinant role in the production of calcium crystals&#44; including hydroxyapatite&#44; as one of our studies has shown&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Although it is a conceptual matter&#44; it should be known that bicarbonate is responsible for the increase in the calcification process&#44; whether directly by causing calcium crystals or indirectly by causing slight alkalinisation&#46; Therefore&#44; bicarbonate should be replaced with another buffering molecule or efforts should be made to reduce it during dialysis&#44; like calcium&#44; obviously within the available means&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">RVB is economically supported by a project &#40;SAF2014-60699-JIN&#41; of the Spanish Ministry of Economics and Competitiveness &#40;MINECO&#41; in association with ERDF funds&#46;</p></span></span>"
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Article information
ISSN: 20132514
Original language: English
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Nefrología (English Edition)