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  <front>
    <journal-meta>
      <journal-id journal-id-type="nlm-ta">Arq Bras Cardiol</journal-id>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id specific-use="scielo-v3" pub-id-type="publisher-id">3XjsXbrhYpxtCxLNc7Ym6fp</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S0066-782X2023001200202</article-id>
      <article-id pub-id-type="other">00202</article-id>
      <article-id pub-id-type="doi">10.36660/abc.20230779</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Minieditorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Rigidez Arterial e Previs&#227;o de Doen&#231;a Renal Cr&#244;nica</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0002-5784-9991</contrib-id>
          <name>
            <surname>Inuzuka</surname>
            <given-names>Sayuri</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
          <xref ref-type="corresp" rid="c1"/>
        </contrib>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0002-1265-1930</contrib-id>
          <name>
            <surname>Barroso</surname>
            <given-names>Weimar Kunz Sebba</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
        </contrib>
        <aff id="aff1">
          <label>1</label>
          <institution content-type="orgname">Universidade Federal de Goi&#225;s</institution>
          <institution content-type="orgdiv1">Liga de Hipertens&#227;o Arterial</institution>
          <addr-line>
            <named-content content-type="city">Goi&#226;nia</named-content>
            <named-content content-type="state">GO</named-content>
          </addr-line>
          <country country="BR">Brasil</country>
          <institution content-type="original">Universidade Federal de Goi&#225;s - Liga de Hipertens&#227;o Arterial, Goi&#226;nia, GO &#8211; Brasil</institution>
        </aff>
        <aff id="aff2">
          <label>2</label>
          <institution content-type="orgname">Universidade Federal de Goi&#225;s</institution>
          <institution content-type="orgdiv1">Faculdade de Medicina</institution>
          <addr-line>
            <named-content content-type="city">Goi&#226;nia</named-content>
            <named-content content-type="state">GO</named-content>
          </addr-line>
          <country country="BR">Brasil</country>
          <institution content-type="original">Faculdade de Medicina - Universidade Federal de Goi&#225;s (UFG), Goi&#226;nia, GO &#8211; Brasil</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c1"><bold>Correspond&#234;ncia: Sayuri Inuzuka</bold> &#8226; Universidade Federal de Goi&#225;s &#8211; Rua 235 QD. 68. CEP <postal-code>74605-050</postal-code>, Lote &#193;rea, Goi&#226;nia, GO &#8211; Brasil E-mail: <email>sa.inuzuka@gmail.com</email></corresp>
      </author-notes>
      <pub-date publication-format="electronic" date-type="pub">
        <day>04</day>
        <month>03</month>
        <year>2024</year>
      </pub-date>
      <pub-date publication-format="electronic" date-type="collection">
        <year>2023</year>
      </pub-date>
      <volume>120</volume>
      <issue>12</issue>
      <elocation-id>e20230779</elocation-id>
      <history>
        <date date-type="received">
          <day>09</day>
          <month>11</month>
          <year>2023</year>
        </date>
        <date date-type="rev-recd">
          <day>06</day>
          <month>12</month>
          <year>2023</year>
        </date>
        <date date-type="accepted">
          <day>06</day>
          <month>12</month>
          <year>2023</year>
        </date>
      </history>
      <permissions>
        <license license-type="open-access" xml:lang="en" xlink:href="https://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License</license-p>
        </license>
      </permissions>
      <kwd-group xml:lang="pt">
        <title>Palavras-chave</title>
        <kwd>Rigidez Arterial</kwd>
        <kwd>Insufici&#234;ncia Renal Cr&#244;nica</kwd>
        <kwd>Hipertens&#227;o</kwd>
        <kwd>Endot&#233;lio Vascular</kwd>
        <kwd>Fatores de Risco</kwd>
      </kwd-group>
      <counts>
        <fig-count count="0"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="13"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>Os sistemas renal e cardiovascular t&#234;m uma liga&#231;&#227;o funcional e essa intera&#231;&#227;o tem recebido aten&#231;&#227;o crescente. A rigidez arterial est&#225; frequentemente associada &#224; doen&#231;a renal cr&#244;nica (DRC), e ambas as condi&#231;&#245;es podem agravar-se mutuamente, gerando e aumentando o risco de eventos cardiovasculares e mortalidade.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Existe um caminho de m&#227;o dupla entre rigidez arterial e disfun&#231;&#227;o renal. O aumento da rigidez arterial e o endot&#233;lio disfuncional ativam citocinas que favorecem eventos tromb&#243;ticos, e c&#233;lulas dendr&#237;ticas e linf&#243;citos potencializam a s&#237;ntese de citocinas pr&#243;-aterog&#234;nicas.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> A inflama&#231;&#227;o vascular amplificada pela DRC estimula o enrijecimento dos vasos pela prolifera&#231;&#227;o das c&#233;lulas musculares lisas vasculares e pela fibrose.<sup><xref ref-type="bibr" rid="B2">2</xref></sup></p>
    <p>Dessa maneira, para tentar responder ao dilema sobre o que veio primeiro, o estudo de C&#226;ndido et al.<sup><xref ref-type="bibr" rid="B3">3</xref></sup> investigou a rela&#231;&#227;o entre o enrijecimento arterial medido pela velocidade da onda de pulso carot&#237;deo-femoral (VOPcf) e a DRC. Esse estudo longitudinal acompanhou 11.647 participantes do estudo ELSA-Brasil durante 4 anos. Os pesquisadores conclu&#237;ram que uma VOPcf mais alta aumentou as chances de DRC em 42% e sugeriram que entre participantes normotensos e n&#227;o diab&#233;ticos esse efeito era ainda mais pronunciado, indicando que a rigidez arterial poderia ser um fator de risco significativo para a DRC, independentemente dessas condi&#231;&#245;es.</p>
    <p>O aumento da VOP e da press&#227;o arterial sist&#243;lica central t&#234;m sido identificados como preditores independentes de futuros eventos cardiovasculares e les&#245;es de &#243;rg&#227;os-alvo, como hipertrofia ventricular esquerda e aumento da microalbumin&#250;ria, e representam os limites entre fatores de risco cardiovascular e eventos cardiovasculares.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> O Systolic Blood Pressure Intervention Trial (SPRINT) concluiu que a press&#227;o arterial sist&#243;lica &lt; 120mmHg n&#227;o foi capaz de reduzir a progress&#227;o da DRC, mas reduziu o risco cardiovascular e a mortalidade em adultos sem diabetes,<sup><xref ref-type="bibr" rid="B5">5</xref></sup> mostrando a natureza multifatorial da progress&#227;o da DRC. O estudo CRIC mostrou que a VOP estava altamente associada &#224; doen&#231;a cardiovascular prevalente e essa associa&#231;&#227;o era independente da press&#227;o arterial sist&#243;lica.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> O Framingham Heart Study avaliou 7.283 indiv&#237;duos por 15 anos e verificou que um incremento do desvio padr&#227;o na VOPcf estava associado a um risco aumentado de DRC (1,19, intervalo de confian&#231;a de 95% 1,05 a 1,34),<sup><xref ref-type="bibr" rid="B7">7</xref></sup> mostrando um resultado semelhante a outros estudos longitudinais.<sup><xref ref-type="bibr" rid="B8">8</xref>,<xref ref-type="bibr" rid="B9">9</xref></sup></p>
    <p>Evid&#234;ncias atuais indicam enrijecimento arterial acelerado em crian&#231;as com DRC, mas n&#227;o h&#225; explica&#231;&#227;o exata para seus mecanismos e consequ&#234;ncias.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> Existe uma rela&#231;&#227;o alinhada com o aumento do risco cardiovascular e anormalidades estruturais do ventr&#237;culo esquerdo.<sup><xref ref-type="bibr" rid="B11">11</xref>,<xref ref-type="bibr" rid="B12">12</xref></sup> Existem m&#250;ltiplas raz&#245;es para esse processo, incluindo press&#227;o arterial elevada, ativa&#231;&#227;o do sistema renina-angiotensina, altera&#231;&#245;es na matriz extracelular vascular, produtos finais de glica&#231;&#227;o avan&#231;ada, estresse oxidativo, disfun&#231;&#227;o endotelial, calcifica&#231;&#227;o vascular e dist&#250;rbios metab&#243;licos &#243;sseos e minerais.<sup><xref ref-type="bibr" rid="B11">11</xref>,<xref ref-type="bibr" rid="B12">12</xref></sup> Claramente, a DRC e o aumento da VOP est&#227;o intimamente interligados e podem influenciar-se mutuamente de maneira bidirecional.<sup><xref ref-type="bibr" rid="B13">13</xref></sup></p>
    <p>Portanto, a rela&#231;&#227;o rec&#237;proca entre o aumento da rigidez arterial e a DRC ressalta a intrincada intera&#231;&#227;o entre a sa&#250;de renal e cardiovascular. O monitoramento da VOP, juntamente com outros fatores de risco cardiovasculares cl&#225;ssicos, pode ser importante na identifica&#231;&#227;o de indiv&#237;duos com maior risco de desenvolver DRC e outras condi&#231;&#245;es relacionadas. A detec&#231;&#227;o precoce e o manejo da rigidez arterial s&#227;o importantes na preven&#231;&#227;o da progress&#227;o das doen&#231;as cardiovasculares e suas complica&#231;&#245;es. Esses marcadores e preditores podem ajudar os profissionais de sa&#250;de a avaliar e gerenciar a sa&#250;de cardiovascular de forma eficaz.</p>
  </body>
  <back>
    <fn-group>
      <fn fn-type="other" id="fn1">
        <p>Minieditorial referente ao artigo: Maior Rigidez Arterial Prediz Doen&#231;a Renal Cr&#244;nica no Estudo de Coorte ELSA-Brasil</p>
      </fn>
    </fn-group>
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  <sub-article article-type="translation" id="S1" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Short Editorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Arterial Stiffness and Chronic Kidney Disease Prediction</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0002-5784-9991</contrib-id>
          <name>
            <surname>Inuzuka</surname>
            <given-names>Sayuri</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>1</sup>
          </xref>
          <xref ref-type="corresp" rid="c2"/>
        </contrib>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0002-1265-1930</contrib-id>
          <name>
            <surname>Barroso</surname>
            <given-names>Weimar Kunz Sebba</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>1</sup>
          </xref>
          <xref ref-type="aff" rid="aff4">
            <sup>2</sup>
          </xref>
        </contrib>
        <aff id="aff3">
          <label>1</label>
          <addr-line>
            <named-content content-type="city">Goi&#226;nia</named-content>
            <named-content content-type="state">GO</named-content>
          </addr-line>
          <country country="BR">Brazil</country>
          <institution content-type="original">Universidade Federal de Goi&#225;s - Liga de Hipertens&#227;o Arterial, Goi&#226;nia, GO &#8211; Brazil</institution>
        </aff>
        <aff id="aff4">
          <label>2</label>
          <addr-line>
            <named-content content-type="city">Goi&#226;nia</named-content>
            <named-content content-type="state">GO</named-content>
          </addr-line>
          <country country="BR">Brazil</country>
          <institution content-type="original">Faculdade de Medicina - Universidade Federal de Goi&#225;s (UFG), Goi&#226;nia, GO &#8211; Brazil</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c2"><bold>Mailing Address: Sayuri Inuzuka</bold> &#8226; Universidade Federal de Goi&#225;s &#8211; Rua 235 QD. 68. Postal Code <postal-code>74605-050</postal-code>, Lote &#193;rea, Goi&#226;nia, GO &#8211; Brasil E-mail: <email>sa.inuzuka@gmail.com</email></corresp>
      </author-notes>
      <kwd-group xml:lang="en">
        <title>Keywords</title>
        <kwd>Arterial Stiffness</kwd>
        <kwd>Kidney Diseases</kwd>
        <kwd>Hypertension</kwd>
        <kwd>Endothelium</kwd>
        <kwd>Risk Factors</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>The kidney and the cardiovascular system have a functional connection, and this interaction has received increasing attention. Arterial stiffness is often associated with chronic kidney disease (CKD), and both conditions can aggravate each other, generating and increasing the risk of cardiovascular events and mortality.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> There is a two-way path between arterial stiffness and renal dysfunction. Increased arterial stiffness and the dysfunctional endothelium activate cytokines that favors thrombotic events, and dendritic cells and lymphocytes enhance the synthesis of pro-atherogenic cytokines.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> The vascular inflammation amplified by CKD stimulates vessel stiffening by proliferation of the vascular smooth muscle cells and fibrosis.<sup><xref ref-type="bibr" rid="B2">2</xref></sup></p>
      <p>Thus, to attempt to answer the dilemma of which came first, the study by C&#226;ndido et al.<sup><xref ref-type="bibr" rid="B3">3</xref></sup> investigated the relationship between arterial stiffening by carotid-femoral pulse wave velocity (cfPWV) and CKD. This longitudinal study followed up 11,647 participants of the ELSA-Brasil study for 4 years. The researchers concluded that higher cfPWV increased the chances of CKD in 42% and suggested that among normotensive, non-diabetic participants, this effect was even more pronounced, indicating that arterial stiffness could be a significant risk factor for CKD independent of these conditions.</p>
      <p>Increased PWV and central systolic blood pressure have been identified as independent predictors of future cardiovascular events and target organ lesions, such as left ventricular hypertrophy and increased microalbuminuria, and they represent the limits between cardiovascular risk factors and cardiovascular events.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> The Systolic Blood Pressure Intervention Trial (SPRINT) concluded that systolic blood pressure &lt; 120mmHg was not able to reduce CKD progression, but it reduced cardiovascular risk and mortality in adults without diabetes,<sup><xref ref-type="bibr" rid="B5">5</xref></sup> showing the multifactorial nature of CKD progression. The CRIC study showed that PWV was highly associated with prevalent cardiovascular disease and this association was independent of systolic blood pressure.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> The Framingham Heart Study evaluated 7,283 subjects for 15 years, found that a standard deviation increment in cfPWV was associated with increased risk of CKD (1.19, 95% confidence interval 1.05 to 1.34),<sup><xref ref-type="bibr" rid="B7">7</xref></sup> showing a similar result to other longitudinal studies.<sup><xref ref-type="bibr" rid="B8">8</xref>,<xref ref-type="bibr" rid="B9">9</xref></sup></p>
      <p>Current evidence indicates accelerated arterial stiffening in children with CKD, but there is no exact explanation for its mechanisms and consequences.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> There is a relationship aligned with increasing cardiovascular risk and left ventricular structural abnormalities.<sup><xref ref-type="bibr" rid="B11">11</xref>,<xref ref-type="bibr" rid="B12">12</xref></sup> There are multiple reasons for this process, including high blood pressure, activation of the renin-angiotensin system, alterations in the vascular extracellular matrix, advanced glycation end products, oxidative stress, endothelial dysfunction, vascular calcification, and metabolic bone and mineral disorders.<sup><xref ref-type="bibr" rid="B11">11</xref>,<xref ref-type="bibr" rid="B12">12</xref></sup> Clearly, CKD and increased PWV are closely interconnected and can influence each other in a bidirectional manner.<sup><xref ref-type="bibr" rid="B13">13</xref></sup></p>
      <p>Therefore, the reciprocal relationship between increased arterial stiffness and CKD underscores the intricate interplay among renal and cardiovascular health. Monitoring PWV, along with other cardiovascular classical risk factors, can be important in identifying individuals at higher risk of developing CKD and other related conditions. Early detection and management of arterial stiffness are significant in preventing the progression of cardiovascular diseases and their complications. These markers and predictors can help healthcare professionals evaluate and manage cardiovascular health effectively.</p>
    </body>
    <back>
      <fn-group>
        <fn fn-type="other" id="fn2">
          <p>Short Editorial related to the article: Higher Arterial Stiffness Predicts Chronic Kidney Disease in Adults: The ELSA-Brasil Cohort Study</p>
        </fn>
      </fn-group>
    </back>
  </sub-article>
</article>
