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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">WYm6C9HTWMkGFCwKwhnPmXG</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S0066-782X2022000400710</article-id>
      <article-id pub-id-type="publisher-id">abc.20220172</article-id>
      <article-id pub-id-type="doi">10.36660/abc.20220172</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Minieditorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Microalbumin&#250;ria e o Risco de Mortalidade em Pacientes com Insufici&#234;ncia Card&#237;aca Aguda</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-7903-8121</contrib-id>
          <name>
            <surname>Beltowski</surname>
            <given-names>Jerzy</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1">
        <label>1</label>
        <institution content-type="orgdiv1">Departamento de Fisiopatologia</institution>
        <institution content-type="orgname">Universidade M&#233;dica de Lublin</institution>
        <addr-line>
          <named-content content-type="city">Lublin</named-content>
        </addr-line>
        <country country="PL">Pol&#244;nia</country>
        <institution content-type="original">Departamento de Fisiopatologia - Universidade M&#233;dica de Lublin, Lublin &#8211; Pol&#244;nia</institution>
      </aff>
      <author-notes>
        <corresp id="c01"> Correspond&#234;ncia: Jerzy Beltowski &#8226; Department of Pathophysiology - Medical University of Lublin - Jaczewskiego 8b 20090 Lublin - Poland E-mail: <email>jerzy.beltowski@umlub.pl</email>; <email>jerzybel@hotmail.com</email> </corresp>
      </author-notes>
      <pub-date date-type="pub" publication-format="electronic">
        <day>29</day>
        <month>04</month>
        <year>2022</year>
      </pub-date>
      <pub-date date-type="collection" publication-format="electronic">
        <month>04</month>
        <year>2022</year>
      </pub-date>
      <volume>118</volume>
      <issue>4</issue>
      <fpage>710</fpage>
      <lpage>711</lpage>
      <permissions>
        <license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/" xml:lang="en">
          <license-p> This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. </license-p>
        </license>
      </permissions>
      <kwd-group xml:lang="pt">
        <kwd>Insufici&#234;ncia Card&#237;aca/fisiopatologia</kwd>
        <kwd>Albuminuria/fisiopatologia</kwd>
        <kwd>Diur&#233;ticos/uso terap&#234;utico</kwd>
        <kwd>Pept&#237;deos Natriur&#233;ticos/uso terap&#234;utico</kwd>
        <kwd>Volume Sist&#243;lico</kwd>
      </kwd-group>
      <counts>
        <fig-count count="0"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="8"/>
        <page-count count="2"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>A insufici&#234;ncia card&#237;aca (IC) &#233; uma s&#237;ndrome cl&#237;nica cr&#244;nica e progressiva resultante de anormalidades estruturais ou funcionais do cora&#231;&#227;o. Os sintomas e sinais mais comuns da IC s&#227;o dispneia, fadiga, congest&#227;o pulmonar e perif&#233;rica ou edema e distens&#227;o da veia jugular. A preval&#234;ncia de IC aumenta continuamente devido &#224; melhoria do tratamento e &#224; redu&#231;&#227;o da mortalidade a curto prazo em pacientes com s&#237;ndromes coronarianas agudas, doen&#231;as card&#237;acas cong&#234;nitas, envelhecimento populacional e melhora da sobrevida de pacientes com insufici&#234;ncia card&#237;aca j&#225; desenvolvida pela ampla aplica&#231;&#227;o de medicamentos modernos modificadores da doen&#231;a e dispositivos.<sup><xref rid="B1" ref-type="bibr">1</xref></sup></p>
    <p>A insufici&#234;ncia card&#237;aca aguda (ICA) &#233; reconhecida quando os sintomas de IC aparecem no paciente sem hist&#243;ria de IC pr&#233;via (IC <italic>de novo</italic>) ou quando os sintomas e sinais est&#227;o se exacerbando rapidamente em um paciente com IC previamente reconhecida (IC descompensada). A insufici&#234;ncia card&#237;aca aguda &#233; a causa mais comum de interna&#231;&#245;es hospitalares n&#227;o planejadas em pacientes idosos. A fisiopatologia de ambas as condi&#231;&#245;es &#233; semelhante, mas a IC <italic>de novo</italic> requer uma abordagem diagn&#243;stica mais detalhada para encontrar a patologia subjacente. O tratamento inicial da ICA inclui diur&#233;ticos intravenosos e vasodilatadores de curta dura&#231;&#227;o. A minoria dos pacientes com ICA apresenta choque cardiog&#234;nico associado a hipotens&#227;o e comprometimento grave da perfus&#227;o dos tecidos perif&#233;ricos; o choque cardiog&#234;nico est&#225; associado a uma mortalidade muito maior do que a ICA sem choque. Enquanto o tratamento da IC cr&#244;nica melhorou substancialmente as taxas de sobrevida, a evolu&#231;&#227;o da ICA ainda &#233; ruim, com altas taxas de mortalidade e reinterna&#231;&#227;o hospitalar. A terapia atualmente usada &#233; direcionada para reduzir a pr&#233; e p&#243;s-carga do cora&#231;&#227;o e n&#227;o visa a patologia subjacente espec&#237;fica em um determinado paciente, o que pode explicar a evolu&#231;&#227;o insatisfat&#243;ria dos resultados cl&#237;nicos. Portanto, a terapia individualizada &#233; muito apreciada, exigindo o estabelecimento de marcadores espec&#237;ficos.<sup><xref rid="B2" ref-type="bibr">2</xref>,<xref rid="B3" ref-type="bibr">3</xref></sup></p>
    <p>Neste n&#250;mero dos Arquivos Brasileiros de Cardiologia, Alata&#351; et al. publicaram um interessante estudo sobre a microalbumin&#250;ria como marcador de mortalidade na ICA.<sup><xref rid="B4" ref-type="bibr">4</xref></sup> Eles analisaram os dados de pacientes adultos admitidos no departamento de emerg&#234;ncia com sinais e sintomas de ICA e aumento do pept&#237;deo natriur&#233;tico cerebral N-terminal (NT-proBNP). Os pacientes foram divididos em tr&#234;s grupos de acordo com a fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo (FEVE): preservada (FEVE &gt;50%, ICFEp), m&#233;dia (FEVE 40-49%, ICFEm) e reduzida (FEVE&lt;40%, ICFEr) incluindo 213, 50 e 63 pacientes, respectivamente. As caracter&#237;sticas demogr&#225;ficas e comorbidades foram coletadas no banco de dados do hospital. A albumin&#250;ria foi definida de acordo com a rela&#231;&#227;o albumina/creatinina urin&#225;ria (RAC): normoalbumin&#250;ria &lt;30 mg/g, microalbumin&#250;ria 30-299 mg/ge macroalbumin&#250;ria &gt;300 mg/g. A m&#233;dia de idade dos pacientes foi de 70,6 anos, sendo 53,3% do sexo feminino. Pacientes com ICFEr apresentaram valores mais elevados de NT-proBNP e RAC do que pacientes com ICFEm ou ICFEp. N&#227;o houve diferen&#231;as significativas na preval&#234;ncia de normo, micro e macroalbumin&#250;ria entre os grupos com ICFEp e ICFEm; no entanto, tanto a micro como a macroalbumin&#250;ria foram mais frequentes na FHrEF do que nos dois grupos restantes. N&#227;o houve diferen&#231;a no tempo de interna&#231;&#227;o entre os grupos. A mortalidade intra-hospitalar foi maior na ICFEr (6,6%) do que na ICFEm (2,0%) ou na ICFEp (2,5%). De acordo com a an&#225;lise multivariada, o NT-proBNP e a macroalbumin&#250;ria estiveram associados &#224; mortalidade intra-hospitalar em todo o grupo. A microalbumin&#250;ria foi associada &#224; mortalidade intra-hospitalar nos grupos ICFEr e ICFEm, mas n&#227;o no grupo ICFEp. O risco de mortalidade hospitalar em pacientes com ICFEr foi 1,94 e 2,45 vezes maior naqueles com micro e macroalbumin&#250;ria, respectivamente, do que naqueles com normoalbumin&#250;ria. Micro e macroalbumin&#250;ria foram associadas a mortalidade 1,56 e 1,92 vezes maior em pacientes com ICFEm.</p>
    <p>A albumin&#250;ria est&#225; associada &#224; IC incidente na popula&#231;&#227;o geral e maior mortalidade entre os pacientes com IC estabelecida.<sup><xref rid="B5" ref-type="bibr">5</xref></sup> No entanto, a rela&#231;&#227;o entre microalbumin&#250;ria e subtipos de IC com FE preservada e reduzida &#233; mais controversa. Ainda menos se sabe sobre a microalbumin&#250;ria como marcador na ICA. Em 2013 Koyama et al.,<sup><xref rid="B6" ref-type="bibr">6</xref></sup> examinaram a evolu&#231;&#227;o da RAC durante a interna&#231;&#227;o em 115 pacientes com IC descompensada.<sup><xref rid="B6" ref-type="bibr">6</xref></sup> Eles observaram uma diminui&#231;&#227;o na preval&#234;ncia de microalbumin&#250;ria e da m&#233;dia da RAC entre os dias 1 e 7 de interna&#231;&#227;o, e essa diminui&#231;&#227;o foi correlacionada com a diminui&#231;&#227;o do NT-proBNP e da bilirrubina s&#233;rica. N&#227;o houve diferen&#231;a na FEVE entre os subgrupos com normo, micro e macroalbumin&#250;ria; no entanto, o NT-proBNP foi significativamente correlacionado com a RAC inicial. No entanto, a rela&#231;&#227;o entre microalbumin&#250;ria e mortalidade n&#227;o foi relatada. Recentemente, Wang et al.,<sup><xref rid="B7" ref-type="bibr">7</xref></sup> examinaram a rela&#231;&#227;o entre a concentra&#231;&#227;o urin&#225;ria de albumina e os resultados em 1.818 pacientes internados no hospital por ICAD. Os pacientes foram acompanhados por um per&#237;odo m&#233;dio de 937,5 dias. A taxa composta de mortalidade, transplante card&#237;aco e implante de dispositivo de assist&#234;ncia ventricular esquerda foi 1,42 e 1,74 vezes maior em pacientes com micro e macroalbumin&#250;ria, respectivamente, do que naqueles sem albumin&#250;ria. Um modelo multivariado de regress&#227;o de Cox incluindo todas as vari&#225;veis significativamente associadas ao progn&#243;stico demonstrou que micro e macroalbumin&#250;ria ainda eram os preditores significativos de mortalidade (taxa de risco 1,27 e 1,36, respectivamente). A an&#225;lise de subgrupo demonstrou que a albumin&#250;ria predisse um risco maior de morte por todas as causas em pacientes com FEVE&gt;40%, mas n&#227;o naqueles com VE&lt;40%. Assim, embora a microalbumin&#250;ria tenha sido associada a pior progn&#243;stico em ambos os estudos,<sup><xref rid="B6" ref-type="bibr">6</xref>,<xref rid="B7" ref-type="bibr">7</xref></sup> essa rela&#231;&#227;o foi mais forte em pacientes com baixa FE no estudo de Alata&#351; et al.,<sup><xref rid="B4" ref-type="bibr">4</xref></sup> e naqueles com maior FE no estudo de Wang et al.,<sup><xref rid="B7" ref-type="bibr">7</xref></sup> A raz&#227;o para essa discrep&#226;ncia n&#227;o &#233; clara, entretanto, v&#225;rias diferen&#231;as entre esses estudos devem ser destacadas. O estudo de Alata&#351; et al.,<sup><xref rid="B4" ref-type="bibr">4</xref></sup> incluiu pacientes com insufici&#234;ncia card&#237;aca aguda (tanto de novo quanto descompensada), idade mais avan&#231;ada (m&#233;dia de 70 anos) e TFGe mais baixa (m&#233;dia de cerca de 70 ml/min) e avaliaram a mortalidade hospitalar. Em contraste, Wang et al.,<sup><xref rid="B7" ref-type="bibr">7</xref></sup> examinaram apenas pacientes com IC descompensada, idade mais jovem (mediana de 57 anos), TFGe mais elevada (m&#233;dia de cerca de 90 ml/min) e avaliaram o desfecho dentro do per&#237;odo mediano de quase 3 anos. Al&#233;m disso, a RAC foi relatado no estudo de Alata&#351; et al.,<sup><xref rid="B4" ref-type="bibr">4</xref></sup> enquanto apenas a concentra&#231;&#227;o absoluta de creatinina urin&#225;ria foi medida por Wang et al.,<sup><xref rid="B7" ref-type="bibr">7</xref></sup> Muito recentemente, Matsumoto et al.,<sup><xref rid="B8" ref-type="bibr">8</xref></sup> demonstraram que o risco de reinterna&#231;&#227;o precoce (dentro de 1 ano) era maior em pacientes com ICAD e micro ou macroalbumin&#250;ria do que naqueles com normoalbumin&#250;ria. Na an&#225;lise multivariada, RAC e BNP foram os preditores independentes de reinterna&#231;&#227;o. No entanto, o valor preditivo da RAC em subgrupos categorizados de acordo com FE n&#227;o foi examinado.<sup><xref rid="B8" ref-type="bibr">8</xref></sup></p>
    <p>Em conclus&#227;o, a microalbumin&#250;ria surge como um novo marcador promissor em pacientes com insufici&#234;ncia card&#237;aca aguda. O estudo de Alata&#351; et al.,<sup><xref rid="B4" ref-type="bibr">4</xref></sup> sugere que a microalbumin&#250;ria seja um preditor de mortalidade intra-hospitalar, principalmente naqueles com fra&#231;&#227;o de eje&#231;&#227;o reduzida. Embora a rela&#231;&#227;o precise entre RAC, FE e outros marcadores, como pept&#237;deos natriur&#233;ticos card&#237;acos, possa diferir dependendo das caracter&#237;sticas dos pacientes e desfechos de interesse, este estudo<sup><xref rid="B4" ref-type="bibr">4</xref></sup> e outros recentes<sup><xref rid="B7" ref-type="bibr">7</xref>,<xref rid="B8" ref-type="bibr">8</xref></sup>abrem uma nova &#225;rea interessante de pesquisa e abordagem cl&#237;nica individualizada.</p>
  </body>
  <back>
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          <article-title>Early evolution and correlates of urine albumin excretion in patients presenting with acutely decompensated heart failure</article-title>
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    <fn-group>
      <fn fn-type="other">
        <p>
          <italic>Minieditorial referente ao artigo: Microalbumin&#250;ria e seu Significado Progn&#243;stico em Pacientes com Insufici&#234;ncia Card&#237;aca Aguda com Fra&#231;&#227;o de Eje&#231;&#227;o Preservada, Intermedi&#225;ria e Reduzida</italic>
        </p>
      </fn>
    </fn-group>
  </back>
  <sub-article article-type="translation" id="TRen" 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>Microalbuminuria and the Risk of Mortality in Patients with Acute Heart Failure</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-7903-8121</contrib-id>
          <name>
            <surname>Beltowski</surname>
            <given-names>Jerzy</given-names>
          </name>
          <xref ref-type="aff" rid="aff1001">
            <sup>1</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1001">
        <label>1</label>
        <country country="PL">Poland</country>
        <institution content-type="original">Departamento de Fisiopatologia - Universidade M&#233;dica de Lublin, Lublin &#8211; Poland</institution>
      </aff>
      <author-notes>
        <corresp id="c01001"> Maling Address: Jerzy Beltowski &#8226; Department of Pathophysiology - Medical University of Lublin - Jaczewskiego 8b 20090 Lublin - Poland E-mail: jerzy.beltowski@umlub.pl; jerzybel@hotmail.com </corresp>
      </author-notes>
      <kwd-group xml:lang="en">
        <kwd>Heart Failure/physiopathology</kwd>
        <kwd>Albuminuria/physiopathology</kwd>
        <kwd>Diuretics/therapeutic use</kwd>
        <kwd>Natriuretic Peptides/therapeutic use</kwd>
        <kwd>Stroke Volume</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>Heart failure (HF) is a chronic and progressive clinical syndrome resulting from structural or functional abnormalities of the heart. The most common symptoms and signs of HF are dyspnea, fatigue, pulmonary and peripheral congestion or edema and jugular vein distension. The prevalence of HF continuously increases due to improved treatment and reduced short-term mortality in patients with acute coronary syndromes, congenital heart disease, population aging and improved survival of patients with already developed heart failure by the widespread application of modern disease-modifying medications and devices.<sup><xref rid="B1" ref-type="bibr">1</xref></sup></p>
      <p>Acute heart failure (AHF) is recognized when symptoms of HF appear in the patient without the history of previous HF (de novo HF) or when symptoms and signs are rapidly exacerbating in a patient with previously recognized HF (decompensated HF). Acute heart failure is the most common cause of unplanned hospital admissions in older patients. The pathophysiology of both conditions is similar, but de novo HF requires a more detailed diagnostic approach to find the underlying pathology. The initial treatment of AHF includes intravenous diuretics and short-acting vasodilators. The minority of patients with AHF present with cardiogenic shock associated with low blood pressure and severely compromised perfusion of peripheral tissues; the cardiogenic shock is associated with much higher mortality than AHF without shock. Whereas the treatment of chronic HF has substantially improved survival rates, the outcome of AHF is still poor, with high mortality and hospital readmission rates. Currently used therapy is directed to reduce the pre and afterload of the heart and does not target the specific underlying pathology in a given patient, which may explain unsatisfactory progress of clinical outcomes. Therefore, individualized therapy is highly appreciated, requiring establishing specific markers.<sup><xref rid="B2" ref-type="bibr">2</xref>,<xref rid="B3" ref-type="bibr">3</xref></sup></p>
      <p>In this issue of the <italic>Brazilian Archives of Cardiology</italic>, Alata&#351; et al. published an interesting study about microalbuminuria as a marker of mortality in AHF.<sup><xref rid="B4" ref-type="bibr">4</xref></sup> They analyzed the data of adult patients admitted to the emergency department with signs and symptoms of AHF and increased N-terminal pro-brain natriuretic peptide (NT-proBNP). Patients were divided into three groups according to left ventricular ejection fraction (LVEF): preserved (LVEF &gt;50%, HFpEF), mid-range (LVEF 40-49%, HFmrEF) and reduced (LVEF&lt;40%, HFrEF) including 213, 50 and 63 patients, respectively. Demographic characteristics and comorbidities were collected from the hospital database. Albuminuria was defined according to urinary albumin-to-creatinine ratio (UACR): normoalbuminuria &lt;30 mg/g, microalbuminuria 30-299 mg/g and macroalbuminuria &gt;300 mg/g. The mean age of patients was 70.6 years, and 53.3% of them were females. Patients with HFrEF had higher NT-proBNP and UACR values than patients with HFmrEF or HFpEF. There were no significant differences in the prevalence of norm-, micro and macroalbuminuria between groups with HFpEF and HFmrEF; however, both micro and macroalbuminuria were more frequent in FHrEF than in the two remaining groups. There was no difference in length of hospital stay between groups. In-hospital mortality was higher in HFrEF (6.6%) than in either HFmrEF (2.0%) or HFpEF (2.5%). According to multivariate analysis, NT-proBNP and macroalbuminuria were associated with in-hospital mortality in the whole group. Microalbuminuria was associated with in-hospital mortality in HFrEF and HFmrEF groups but not in the HFpEF group. The risk of in-hospital mortality in patients with HFrEF was 1,94- and 2.45-fold higher in those with micro and macroalbuminuria, respectively, than in those with normoalbuminuria. Micro and macroalbuminuria were associated with 1.56- and 1.92-fold higher mortality in patients with HFmrEF.</p>
      <p>Albuminuria is associated with incident HF in the general population and higher mortality among patients with established HF.<sup><xref rid="B5" ref-type="bibr">5</xref></sup> However, the relationship between microalbuminuria and HF subtypes with preserved and reduced EF is more controversial. Even less is known about microalbuminuria as a marker in AHF. In 2013 Koyama et al.<sup><xref rid="B6" ref-type="bibr">6</xref></sup> examined the evolution of UACR during hospitalization in 115 patients with decompensated HF.<sup><xref rid="B6" ref-type="bibr">6</xref></sup> They observed a decrease in the prevalence of microalbuminuria and the mean UACR between days 1 and 7 of hospitalization, and this decrease was correlated with the decrease in NT-proBNP and serum bilirubin. There was no difference in LVEF between subgroups with normo, micro and macroalbuminuria; however, NT-proBNP was significantly correlated with baseline UACR. Nevertheless, the relationship between microalbuminuria and mortality was not reported. Recently, Wang et al.<sup><xref rid="B7" ref-type="bibr">7</xref></sup> examined the relationship between urinary albumin concentration and outcomes in 1818 patients admitted to the hospital due to ADHF. The patients were followed for a median period of 937.5 days. The compound rate of mortality, heart transplantation, and left ventricular assist device implantation was 1.42- and 1.74-fold higher in patients with micro and macroalbuminuria, respectively, than in those without albuminuria. A multivariate Cox regression model including all variables significantly associated with prognosis demonstrated that micro and macroalbuminuria were still the significant predictors of mortality (hazard ratio 1.27 and 1.36, respectively). Subgroup analysis demonstrated that albuminuria predicted a higher risk of all-cause death in patients with LVEF&gt;40% but not those with LV&lt;40%. Thus, although microalbuminuria was associated with a worse prognosis in both studies.<sup><xref rid="B6" ref-type="bibr">6</xref>,<xref rid="B7" ref-type="bibr">7</xref></sup> this relationship was stronger in patients with low EF in the study of Alata&#351; et al.<sup><xref rid="B4" ref-type="bibr">4</xref></sup> and in those with higher EF in the study of Wang et al.<sup><xref rid="B7" ref-type="bibr">7</xref></sup> The reason for this discrepancy is unclear, however, several differences between these studies should be highlighted. The study of Alata&#351; et al.<sup><xref rid="B4" ref-type="bibr">4</xref></sup> included patients with acute heart failure (both de novo and decompensated), older age (mean 70 years) and lower eGFR )mean about 70 ml/min) and assessed in-hospital mortality. In contrast, Wang et al.<sup><xref rid="B7" ref-type="bibr">7</xref></sup> examined only patients with decompensated HF, younger age (median 57 years), higher eGFR (mean about 90 ml/min) and assessed the outcome within the median period of almost 3 years. In addition, UACR was reported in the study of Alata&#351; et al.<sup><xref rid="B4" ref-type="bibr">4</xref></sup> whereas only absolute urinary creatinine concentration was measured by Wang et al.<sup><xref rid="B7" ref-type="bibr">7</xref></sup> Very recently, Matsumoto et al.<sup><xref rid="B8" ref-type="bibr">8</xref></sup> demonstrated that the risk of early (within 1 year) rehospitalization was higher in patients with ADHF and micro- or macroalbuminuria than in those with normoalbuminuria. In multivariate analysis, UACR and BNP were the independent predictors of rehospitalization. However, the predictive value of UACR in subgroups categorized according to EF was not examined.<sup><xref rid="B8" ref-type="bibr">8</xref></sup></p>
      <p>In conclusion, microalbuminuria emerges as a novel promising marker in patients with acute heart failure. The study of Alata&#351; et al.<sup><xref rid="B4" ref-type="bibr">4</xref></sup> suggests that microalbuminuria is a predictor of in-hospital mortality, especially in those with reduced ejection fraction. Although the precise relationship between UACR, EF and other markers such as cardiac natriuretic peptides may differ depending on the characteristics of patients and outcomes of interest, this study<sup><xref rid="B4" ref-type="bibr">4</xref></sup> and other recent ones<sup><xref rid="B7" ref-type="bibr">7</xref>,<xref rid="B8" ref-type="bibr">8</xref></sup> open a new interesting area of research and individualized clinical approach.</p>
    </body>
    <back>
      <fn-group>
        <fn id="fn1001">
          <label/>
          <p>
            <italic>Short Editorial related to the article: Microalbuminuria and its Prognostic Significance in Patients with Acute Heart Failure With Preserved, Mid-Range, and Reduced Ejection Fraction</italic>
          </p>
        </fn>
      </fn-group>
    </back>
  </sub-article>
</article>
