<?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>S0211-69952017000100009</article-id>
<article-id pub-id-type="doi">10.1016/j.nefro.2016.05.008</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Microbiota intestinal en la enfermedad renal crónica]]></article-title>
<article-title xml:lang="en"><![CDATA[Gut microbiota in chronic kidney disease]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cigarran Guldris]]></surname>
<given-names><![CDATA[Secundino]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[González Parra]]></surname>
<given-names><![CDATA[Emilio]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cases Amenós]]></surname>
<given-names><![CDATA[Aleix]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital Da Costa Sección de Nefrología ]]></institution>
<addr-line><![CDATA[Burela Lugo]]></addr-line>
<country>España</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Fundación Jiménez Díaz Servicio de Nefrología ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<aff id="Af4">
<institution><![CDATA[,Universidad Autónoma de Madrid  ]]></institution>
<addr-line><![CDATA[Madrid ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Hospital Clinic Servicio de Nefrología ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<aff id="Af5">
<institution><![CDATA[,Universitat de Barcelona  ]]></institution>
<addr-line><![CDATA[Barcelona ]]></addr-line>
<country>Spain</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>9</fpage>
<lpage>19</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_arttext&amp;pid=S0211-69952017000100009&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_abstract&amp;pid=S0211-69952017000100009&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_pdf&amp;pid=S0211-69952017000100009&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La microflora intestinal mantiene una relación simbiótica con el huésped en condiciones normales, sin embargo, su alteración se ha asociado recientemente con numerosas enfermedades. En la enfermedad renal crónica (ERC) se ha descrito una disbiosis en la microflora intestinal con un aumento de la flora patógena sobre la simbionte. Además, la permeabilidad de la barrera intestinal está aumentada, lo que permite el paso de endotoxinas y otros productos bacterianos a la sangre. La microflora intestinal, mediante la fermentación de productos no digeridos que alcanzan el colon, produce indoles, fenoles, o aminas, entre otros, que son absorbidos por el huésped, se acumulan en la ERC y tienen efectos deletéreos sobre el organismo. Estas toxinas urémicas generadas en el intestino y el aumento de la permeabilidad de la barrera intestinal en la ERC se han asociado a un aumento de la inflamación y el estrés oxidativo, y están implicados en diversas complicaciones asociadas a la ERC, como la enfermedad cardiovascular, la anemia, las alteraciones del metabolismo mineral o la progresión de la ERC. El uso de prebióticos, probióticos o simbióticos, entre otras aproximaciones, podrían mejorar la disbiosis o el aumento de la permeabilidad de la barrera intestinal en la ERC. En este artículo se revisan la situación de la microflora intestinal en la ERC, la alteración de la barrera intestinal y sus consecuencias clínicas, los efectos deletéreos de las toxinas urémicas derivadas de la microflora intestinal, así como las posibles opciones terapéuticas para mejorar esta disbiosis y reducir las complicaciones de la ERC.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract The intestinal microflora maintains a symbiotic relationship with the host under normal conditions, but its imbalance has recently been associated with several diseases. In chronic kidney disease (CKD), dysbiotic intestinal microflora has been reported with an increase in pathogenic flora compared to symbiotic flora. An enhanced permeability of the intestinal barrier, allowing the passage of endotoxins and other bacterial products to the blood, has also been shown in CKD. By fermenting undigested products that reach the colon, the intestinal microflora produce indoles, phenols and amines, among others, that are absorbed by the host, accumulate in CKD and have harmful effects on the body. These gut-derived uraemic toxins and the increased permeability of the intestinal barrier in CKD have been associated with increased inflammation and oxidative stress and have been involved in various CKD-related complications, including cardiovascular disease, anaemia, mineral metabolism disorders or the progression of CKD. The use of prebiotics, probiotics or synbiotics, among other approaches, could improve the dysbiosis and/or the increased permeability of the intestinal barrier in CKD. This article describes the situation of the intestinal microflora in CKD, the alteration of the intestinal barrier and its clinical consequences, the harmful effects of intestinal flora-derived uraemic toxins, and possible therapeutic options to improve this dysbiosis and reduce CKD-related complications.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Enfermedad renal crónica]]></kwd>
<kwd lng="es"><![CDATA[Microbiota intestinal]]></kwd>
<kwd lng="es"><![CDATA[Disbiosis]]></kwd>
<kwd lng="es"><![CDATA[Toxinas urémicas]]></kwd>
<kwd lng="es"><![CDATA[Inflamación]]></kwd>
<kwd lng="en"><![CDATA[Chronic kidney disease]]></kwd>
<kwd lng="en"><![CDATA[Gut microbiota]]></kwd>
<kwd lng="en"><![CDATA[Dysbiosis]]></kwd>
<kwd lng="en"><![CDATA[Uraemic toxins]]></kwd>
<kwd lng="en"><![CDATA[Inflammation]]></kwd>
</kwd-group>
</article-meta>
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