<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0211-6995</journal-id>
<journal-title><![CDATA[Nefrología (Madrid)]]></journal-title>
<abbrev-journal-title><![CDATA[Nefrología (Madr.)]]></abbrev-journal-title>
<issn>0211-6995</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Española de Nefrología]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0211-69952017000100005</article-id>
<article-id pub-id-type="doi">10.1016/j.nefro.2016.04.008</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[¿Es el sistema calicreína/quinina renal un factor modulador de la calciuria?]]></article-title>
<article-title xml:lang="en"><![CDATA[Is the renal kallikrein-kinin system a factor that modulates calciuria?]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Negri]]></surname>
<given-names><![CDATA[Armando Luis]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad del Salvador Cátedra de Fisiología y Biofísica ]]></institution>
<addr-line><![CDATA[Buenos Aires ]]></addr-line>
<country>Argentina</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>02</month>
<year>2017</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>02</month>
<year>2017</year>
</pub-date>
<volume>37</volume>
<numero>1</numero>
<fpage>5</fpage>
<lpage>8</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_arttext&amp;pid=S0211-69952017000100005&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_abstract&amp;pid=S0211-69952017000100005&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_pdf&amp;pid=S0211-69952017000100005&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La reabsorción tubular de calcio es uno de los principales factores que determinan la concentración sérica de calcio y su excreción urinaria. El túbulo contorneado distal y conector es donde se produce la regulación fina de la calciuria. A ese nivel se encuentra el canal epitelial de Ca (TRPV5), que es el paso limitante en el transporte transcelular de Ca. La presencia dinámica del canal TRPV5 en la superficie de la célula tubular está mediada por un proceso de reciclado endosómico. Distintos factores intrarrenales intervienen en la fijación del canal de calcio en la membrana aplical, entre ellos la hormona antienvejecimiento klotho y la calicreína tisular (CT). Ambas proteínas son sintetizadas en el túbulo distal y secretadas en el fluido tubular. La calicreína tisular estimula la reabsorción activa de calcio por vía del receptor de bradiquinina tipo 2 que compromete la activación del of TRPV5 por vía de la protein cinasa C. Los ratones deficientes en CT muestran hipercalciuria de origen renal comparable a la pérdida de calcio que se observa en los ratones knockout para el TRPV5. Existe un polimorfismo con pérdida de función del gen de la CT humana denominado R53H (alelo H) que produce una gran disminución de la actividad enzimática. La presencia del alelo H, por lo menos en la población japonesa, parece ser frecuente (24%). Estos individuos tiene una tendencia a excreción más alta de calcio y sodio en orina que se manifiesta más durante la infusión de furosemida. En el futuro habrá que estudiar si la manipulación del sistema calicreína-quinina renal permite corregir la hipercalciuria idiopática con fármacos diferentes a los diuréticos tiazídicos.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Renal tubular calcium reabsorption is one of the principal factors that determine serum calcium concentration and calcium excretion. Calcium excretion is regulated by the distal convoluted tubule and connecting tubule, where the epithelial calcium channel TRPV5 can be found, which limits the rate of transcellular calcium transport. The dynamic presence of the TRPV5 channel on the surface of the tubular cell is mediated by an endosomal recycling process. Different intrarenal factors are involved in calcium channel fixation in the apical membrane, including the anti-ageing hormone klotho and tissue kallikrein (TK). Both proteins are synthesised in the distal tubule and secreted in the tubular fluid. TK stimulates active calcium reabsorption through the bradykinin receptor B2 that compromises TRPV5 activation through the protein kinase C pathway. TK-deficient mice show hypercalciuria of renal origin comparable to that seen in TRPV5 knockout mice. There is a polymorphism with loss of function of the human TK gene R53H (allele H) that causes a marked decrease in enzymatic activity. The presence of the allele H seems to be common at least in the Japanese population (24%). These individuals have a tendency to greater calcium and sodium excretion in urine that is more evident during furosemide infusion. Future studies should analyse if manipulating the renal kallikrein-kinin system can correct idiopathic hypercalciuria with drugs other than thiazide diuretics.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Calicreína tisular]]></kwd>
<kwd lng="es"><![CDATA[Calciuria]]></kwd>
<kwd lng="es"><![CDATA[Regulación]]></kwd>
<kwd lng="en"><![CDATA[Tissue kallikrein]]></kwd>
<kwd lng="en"><![CDATA[Calciuria]]></kwd>
<kwd lng="en"><![CDATA[Regulation]]></kwd>
</kwd-group>
</article-meta>
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