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    "titulo" => "Looking at the clock of kidney dysfunction"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Heart and kidney walk side by side along the path of heart failure &#40;HF&#41;&#46; Chronic kidney disease &#40;CKD&#41; is highly prevalent and has a similar impact on prognosis among HF patients regardless of ejection fraction&#46; CKD is present in up to 50&#37; of HF patients and increases their risk of death to 25&#37; at one year&#46; HF patients with CKD are normally older&#44; have more comorbidities and are more symptomatic than HF patients without CKD&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The complex hemodynamic and neurohormonal interaction between the heart and kidney gave rise to the concept of the cardiorenal syndrome&#44; in which dysfunction of one organ induces or aggravates dysfunction in the other&#44; impacting on each other&#39;s prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">3</span></a> Renal dysfunction in HF is a consequence of the complex interaction between hemodynamic factors&#44; systemic congestion&#44; inflammation&#44; endothelial dysfunction&#44; and neurohormonal mechanisms&#46; A reduction in cardiac output in patients with chronic HF has been shown to result in a decrease in renal blood flow&#44; activating renal mechanisms that result in water and sodium retention and thereby causing congestion&#46; This congestion further worsens HF but also leads to an increase in central venous or abdominal pressure&#44; which ultimately causes worsening renal function &#40;WRF&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">In acute heart failure &#40;AHF&#41;&#44; congestion is the main clinical presentation&#44; and therefore WRF is prevalent among AHF patients&#46; In their study published in this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Presume et al&#46; assess the prognosis of AHF patients according to the time of WRF onset&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> Unlike the majority of works on this subject&#44; the authors aim to identify the prognostic value of WRF according to the time of its occurrence during a HF decompensation episode&#46; WRF was defined as an increase in serum creatine &#40;SCr&#41; of &#62;0&#46;3 mg&#47;dl&#46; If WRF occurred within the six months before admission&#44; it was classified as acute kidney injury &#40;AKI&#41;&#46; During hospitalization for HF&#44; WRF was analyzed in patients with or without AKI at admission&#44; who were classified as having early &#40;&#8804;48 hours&#41; or late &#40;&#62;48 hours&#41; WRF&#46; Studying a total of 249 patients&#44; of whom 62&#46;2&#37; had preserved left ventricular ejection fraction and 55&#46;8&#37; had CKD&#44; the authors found that WRF was a stronger predictor of worse prognosis at one year &#40;hazard ratio &#91;HR&#93; 1&#46;69&#59; 95&#37; confidence interval &#91;CI&#93; 1&#46;15&#8211;2&#46;48&#59; p&#61;0&#46;007&#41;&#46; In particular&#44; early WRF was associated with a significantly higher incidence of the primary outcome &#40;HR 2&#46;49&#59; 95&#37; CI 1&#46;66&#8211;3&#46;73&#59; p&#60;0&#46;001&#41;&#44; whereas late WRF was not &#40;HR 0&#46;80&#59; 95&#37; CI 0&#46;45&#8211;1&#46;40&#59; p&#61;0&#46;411&#41;&#44; compared to patients who did not develop WRF&#46; The outcome at one&#44; three and six months was also worse for patients who developed early WRF&#44; as length of hospital stay was longer&#46; Interestingly&#44; AKI at admission was not an independent predictor of the primary outcome&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">These results illustrate common beliefs concerning the prognostic impact of WRF in AHF patients&#46; Nevertheless&#44; the evidence is conflicting&#44; and some studies show that WRF during hospitalization for HF is a less important predictor of events than AKI at admission&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">6&#44;7</span></a> Others&#44; even from the same authors&#44; emphasize the impact of early AKI during hospitalization for HF&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">8</span></a> But in all these works&#44; the time frame for recording the onset of WRF during hospitalization for HF was longer&#44; around five days after admission&#46; Also&#44; the prevalence of HF patients with preserved ejection fraction &#40;HFpEF&#41; in these studies was considerably lower than in the present study population&#44; in which HFpEF prevalence was 62&#46;2&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">5&#8211;7</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">In Presume et al&#46;&#8217;s study&#44; WRF during hospitalization for HF was more important than AKI at admission&#44; and early WRF was the main predictor of post-discharge prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> This may reflect the different pathophysiological mechanisms of WRF during AHF&#44; of which intra-abdominal &#40;visceral and&#47;or renal&#41; congestion may be among the most important&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">4</span></a> Prompt diuretic therapy for decongestion or improvement of perfusion by increasing cardiac output are the strategies for congestive patients &#40;warm-wet &#91;type B&#93; and cold-wet &#91;type C&#93; hemodynamic profiles&#41;&#46; Improvement of AKI present at admission is the most frequent result of an efficacious decongestive approach to the AHF patient&#46; Unfortunately&#44; effective decongestion is difficult to achieve and WRF arises as congestion persists or worsens&#46; One possible explanation for Presume et al&#46;&#8217;s results is that early WRF is a marker of unsuccessful decongestion and is therefore associated with a worse prognosis&#46; By contrast&#44; late WRF may reflect the effects of diuretic therapy leading to excessive reduction of preload and systemic hypoperfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">9</span></a> Ahmad et al&#46; found that aggressive diuretic strategies&#44; observed WRF and increases in tubular injury biomarkers at 72 hours were not associated with adverse outcomes but rather with a paradoxical trend toward improved outcomes&#46; These declines in estimated glomerular filtration rate &#40;eGFR&#41; likely represent clinically benign changes in filtration rather than a manifestation of tubular injury to the kidney&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">10</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Data on urine output and characteristics &#40;such as natriuresis&#41; that are missing in Presume et al&#46;&#8217;s study<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> could have shed more light on the pathophysiology underlying early WRF&#44; revealing whether these patients might have had an inadequate response to diuretic therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> Similarly&#44; data on weight loss and changes in natriuretic peptides&#44; and even assessment of patients&#8217; symptomatic and hemodynamic status&#44; would have brought more insight&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">After discharge&#44; prognosis is greatly influenced by prognosis-modifying therapy&#44; especially in HF patients with reduced ejection fraction &#40;HFrEF&#41;&#46; In Presume et al&#46;&#8217;s study&#44; patients with HFrEF were well medicated at discharge&#44; with 75&#46;8&#37; on angiotensin-converting enzyme inhibitors&#47;angiotensin receptor blockers&#44; 72&#46;7&#37; on beta-blockers and 53&#46;0&#37; on mineralocorticoid receptor antagonists&#46; But the fear of hyperkalemia or of further deterioration in renal function often makes physicians reluctant to initiate or to titrate agents acting on the renin-angiotensin-aldosterone system &#40;RAAS&#41; and the sympathetic system&#44;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">11</span></a> the main treatment for HFrEF&#44; during hospitalization for HF&#46; Therefore&#44; HF patients with concomitant CKD are less likely to receive new guideline-recommended therapies&#46; Nevertheless&#44; in the majority of HF trials targeting the RAAS&#44; benefits were observed regardless of the presence of CKD&#44; even though patients with more severe CKD &#40;SCr &#62;2&#46;5 mg&#47;dl or eGFR &#60;30 ml&#47;min&#47;1&#46;73 m<span class="elsevierStyleSup">2</span>&#41; were excluded&#46; Furthermore&#44; recent trials with sacubitril&#47;valsartan and sodium&#47;glucose cotransporter 2 &#40;SGLT2&#41; inhibitors&#44; along with cardiovascular benefits&#44; demonstrated improved renal outcomes&#44; slowing the rate of decrease in eGFR&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">6</span></a> It is important to remember that initiation of SGLT-2 inhibitors is associated with an initial transient and mild fall in eGFR over the first weeks&#46; This initial mild drop in eGFR should not lead to premature discontinuation of SGLT-2 inhibitor therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">11</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Presume et al&#46;&#8217;s study illustrates a latent concept that could be called the &#8216;chronological phenotyping of WRF&#8217;&#46; When dealing with an AHF episode&#44; physicians should be looking further into the clock of kidney dysfunction&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Looking at the clock of kidney dysfunction
O relógio da disfunção renal na insuficiência cardíaca aguda…
Pedro Morais Sarmento
Hospital da Luz Lisboa, Heart Failure Outpatient Clinic, Department of Internal Medicine, Lisboa, Portugal
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Heart and kidney walk side by side along the path of heart failure &#40;HF&#41;&#46; Chronic kidney disease &#40;CKD&#41; is highly prevalent and has a similar impact on prognosis among HF patients regardless of ejection fraction&#46; CKD is present in up to 50&#37; of HF patients and increases their risk of death to 25&#37; at one year&#46; HF patients with CKD are normally older&#44; have more comorbidities and are more symptomatic than HF patients without CKD&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The complex hemodynamic and neurohormonal interaction between the heart and kidney gave rise to the concept of the cardiorenal syndrome&#44; in which dysfunction of one organ induces or aggravates dysfunction in the other&#44; impacting on each other&#39;s prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">3</span></a> Renal dysfunction in HF is a consequence of the complex interaction between hemodynamic factors&#44; systemic congestion&#44; inflammation&#44; endothelial dysfunction&#44; and neurohormonal mechanisms&#46; A reduction in cardiac output in patients with chronic HF has been shown to result in a decrease in renal blood flow&#44; activating renal mechanisms that result in water and sodium retention and thereby causing congestion&#46; This congestion further worsens HF but also leads to an increase in central venous or abdominal pressure&#44; which ultimately causes worsening renal function &#40;WRF&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">In acute heart failure &#40;AHF&#41;&#44; congestion is the main clinical presentation&#44; and therefore WRF is prevalent among AHF patients&#46; In their study published in this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Presume et al&#46; assess the prognosis of AHF patients according to the time of WRF onset&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> Unlike the majority of works on this subject&#44; the authors aim to identify the prognostic value of WRF according to the time of its occurrence during a HF decompensation episode&#46; WRF was defined as an increase in serum creatine &#40;SCr&#41; of &#62;0&#46;3 mg&#47;dl&#46; If WRF occurred within the six months before admission&#44; it was classified as acute kidney injury &#40;AKI&#41;&#46; During hospitalization for HF&#44; WRF was analyzed in patients with or without AKI at admission&#44; who were classified as having early &#40;&#8804;48 hours&#41; or late &#40;&#62;48 hours&#41; WRF&#46; Studying a total of 249 patients&#44; of whom 62&#46;2&#37; had preserved left ventricular ejection fraction and 55&#46;8&#37; had CKD&#44; the authors found that WRF was a stronger predictor of worse prognosis at one year &#40;hazard ratio &#91;HR&#93; 1&#46;69&#59; 95&#37; confidence interval &#91;CI&#93; 1&#46;15&#8211;2&#46;48&#59; p&#61;0&#46;007&#41;&#46; In particular&#44; early WRF was associated with a significantly higher incidence of the primary outcome &#40;HR 2&#46;49&#59; 95&#37; CI 1&#46;66&#8211;3&#46;73&#59; p&#60;0&#46;001&#41;&#44; whereas late WRF was not &#40;HR 0&#46;80&#59; 95&#37; CI 0&#46;45&#8211;1&#46;40&#59; p&#61;0&#46;411&#41;&#44; compared to patients who did not develop WRF&#46; The outcome at one&#44; three and six months was also worse for patients who developed early WRF&#44; as length of hospital stay was longer&#46; Interestingly&#44; AKI at admission was not an independent predictor of the primary outcome&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">These results illustrate common beliefs concerning the prognostic impact of WRF in AHF patients&#46; Nevertheless&#44; the evidence is conflicting&#44; and some studies show that WRF during hospitalization for HF is a less important predictor of events than AKI at admission&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">6&#44;7</span></a> Others&#44; even from the same authors&#44; emphasize the impact of early AKI during hospitalization for HF&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">8</span></a> But in all these works&#44; the time frame for recording the onset of WRF during hospitalization for HF was longer&#44; around five days after admission&#46; Also&#44; the prevalence of HF patients with preserved ejection fraction &#40;HFpEF&#41; in these studies was considerably lower than in the present study population&#44; in which HFpEF prevalence was 62&#46;2&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">5&#8211;7</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">In Presume et al&#46;&#8217;s study&#44; WRF during hospitalization for HF was more important than AKI at admission&#44; and early WRF was the main predictor of post-discharge prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> This may reflect the different pathophysiological mechanisms of WRF during AHF&#44; of which intra-abdominal &#40;visceral and&#47;or renal&#41; congestion may be among the most important&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">4</span></a> Prompt diuretic therapy for decongestion or improvement of perfusion by increasing cardiac output are the strategies for congestive patients &#40;warm-wet &#91;type B&#93; and cold-wet &#91;type C&#93; hemodynamic profiles&#41;&#46; Improvement of AKI present at admission is the most frequent result of an efficacious decongestive approach to the AHF patient&#46; Unfortunately&#44; effective decongestion is difficult to achieve and WRF arises as congestion persists or worsens&#46; One possible explanation for Presume et al&#46;&#8217;s results is that early WRF is a marker of unsuccessful decongestion and is therefore associated with a worse prognosis&#46; By contrast&#44; late WRF may reflect the effects of diuretic therapy leading to excessive reduction of preload and systemic hypoperfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">9</span></a> Ahmad et al&#46; found that aggressive diuretic strategies&#44; observed WRF and increases in tubular injury biomarkers at 72 hours were not associated with adverse outcomes but rather with a paradoxical trend toward improved outcomes&#46; These declines in estimated glomerular filtration rate &#40;eGFR&#41; likely represent clinically benign changes in filtration rather than a manifestation of tubular injury to the kidney&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">10</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Data on urine output and characteristics &#40;such as natriuresis&#41; that are missing in Presume et al&#46;&#8217;s study<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> could have shed more light on the pathophysiology underlying early WRF&#44; revealing whether these patients might have had an inadequate response to diuretic therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a> Similarly&#44; data on weight loss and changes in natriuretic peptides&#44; and even assessment of patients&#8217; symptomatic and hemodynamic status&#44; would have brought more insight&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">After discharge&#44; prognosis is greatly influenced by prognosis-modifying therapy&#44; especially in HF patients with reduced ejection fraction &#40;HFrEF&#41;&#46; In Presume et al&#46;&#8217;s study&#44; patients with HFrEF were well medicated at discharge&#44; with 75&#46;8&#37; on angiotensin-converting enzyme inhibitors&#47;angiotensin receptor blockers&#44; 72&#46;7&#37; on beta-blockers and 53&#46;0&#37; on mineralocorticoid receptor antagonists&#46; But the fear of hyperkalemia or of further deterioration in renal function often makes physicians reluctant to initiate or to titrate agents acting on the renin-angiotensin-aldosterone system &#40;RAAS&#41; and the sympathetic system&#44;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">11</span></a> the main treatment for HFrEF&#44; during hospitalization for HF&#46; Therefore&#44; HF patients with concomitant CKD are less likely to receive new guideline-recommended therapies&#46; Nevertheless&#44; in the majority of HF trials targeting the RAAS&#44; benefits were observed regardless of the presence of CKD&#44; even though patients with more severe CKD &#40;SCr &#62;2&#46;5 mg&#47;dl or eGFR &#60;30 ml&#47;min&#47;1&#46;73 m<span class="elsevierStyleSup">2</span>&#41; were excluded&#46; Furthermore&#44; recent trials with sacubitril&#47;valsartan and sodium&#47;glucose cotransporter 2 &#40;SGLT2&#41; inhibitors&#44; along with cardiovascular benefits&#44; demonstrated improved renal outcomes&#44; slowing the rate of decrease in eGFR&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">6</span></a> It is important to remember that initiation of SGLT-2 inhibitors is associated with an initial transient and mild fall in eGFR over the first weeks&#46; This initial mild drop in eGFR should not lead to premature discontinuation of SGLT-2 inhibitor therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">11</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Presume et al&#46;&#8217;s study illustrates a latent concept that could be called the &#8216;chronological phenotyping of WRF&#8217;&#46; When dealing with an AHF episode&#44; physicians should be looking further into the clock of kidney dysfunction&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Revista Portuguesa de Cardiologia
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Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos

Ao assinalar que é «Profissional de Saúde», declara conhecer e aceitar que a responsável pelo tratamento dos dados pessoais dos utilizadores da página de internet da Revista Portuguesa de Cardiologia (RPC), é esta entidade, com sede no Campo Grande, n.º 28, 13.º, 1700-093 Lisboa, com os telefones 217 970 685 e 217 817 630, fax 217 931 095 e com o endereço de correio eletrónico revista@spc.pt. Declaro para todos os fins, que assumo inteira responsabilidade pela veracidade e exatidão da afirmação aqui fornecida.