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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Contrast-induced nephropathy &#40;CIN&#41; is a major concern in daily practice for everyone working in interventional cardiology&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The use of contrast agents has been growing due to the increasing number of procedures that use them&#44; such as&#58; structural heart therapies and primary angioplasty for ST-segment elevation myocardial infarction &#40;STEMI&#41;&#46; Contrast-induced nephropathy has a major impact on prognosis after primary percutaneous coronary intervention &#40;PCI&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1&#44;2</span></a> In this particular setting&#44; it is problematic due to the clinical instability of the patient and the impossibility of prevention in an emerging situation&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Contrast-induced nephropathy is a well-known cause of acute renal failure but the underlying mechanisms are yet to be fully understood&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The evidence is in favor of a combination of direct toxic effects on tubular epithelial cells and renal ischemia as the pathogenetic role&#46; The generation of reactive oxygen species&#44; which in turn scavenge nitric oxide&#44; further increases hypoxia&#46;<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">4&#44;5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Identified risk factors for CIN are the baseline renal function itself&#44; diabetes&#44; acute myocardial infarction&#44; shock and the volume of contrast medium administered during the procedure&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">4</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Among patients with STEMI&#44; the role of contrast agents has been questioned in acute kidney injury &#40;AKI&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> In this study&#44; Caspi et al&#46; concluded that the risk for AKI was similar among STEMI patients regardless of exposure to contrast material&#46; Independent predictors of AKI in patients who underwent primary PCI included age &#8805;70 years&#44; insulin-treated diabetes&#44; diuretic therapy&#44; previous infarction&#44; baseline estimated glomerular filtration rate&#44; and variables related to the presence of pump failure &#40;higher Killip class&#44; intra-aortic balloon pump use&#41; and reduced left ventricular ejection fraction but not contrast agent dose&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In this issue Fatih Aksoy et al&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> assessed the association between total oxidant status &#40;TOS&#41;&#44; total antioxidant capacity &#40;TAC&#41; and CIN in patients with STEMI&#46; They assessed a cohort of 341 patients&#46; In a multivariate regression analysis&#44; they concluded that high-sensitivity C-reactive protein&#44; uric acid and oxidative status index predicted the development of CIN&#46; They also suggest that incorporating these variables into existing risk scores like the Mehran risk score<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">8</span></a> could improve its accuracy&#46; Nevertheless&#44; only 16&#46;7&#37; of these patients developed CIN&#44; which the authors acknowledged could have influenced their results&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The results suggest&#44; nonetheless&#44; that TOC&#44; TAC and oxidative stress index are associated with the development of CIN&#44; reinforcing the possibility that oxidative stress may be partially responsible for the development of CIN&#44; as already suggested by others&#46;<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9&#44;10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Preventive measures for CIN&#44; such as fluid administration&#44; pharmacological strategies&#44; use of different contrast agents and renal replacement therapies&#44; have been extensively assessed in many trials&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">There seems to be some consensus on fluid administration as a means of protecting from CIN&#44; but the results from trials are conflicting&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">11&#44;12</span></a> The addition of sodium bicarbonate may provide additional kidney protection by alkalinizing renal tubular fluid and thereby minimizing tubular damage&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">13</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Fluid administration possibly associated with furosemide forced diuresis seems to be a good strategy&#44; although there is the risk of hypovolemia&#46; The fear of giving too much volume&#44; mainly in patients with low ejection fraction can&#44; on the other hand&#44; lead to suboptimal protection&#46; Renal Guard&#44; a device enabling volume administration to be balanced with urine output&#44; showed that a high urine output was achievable&#44; while avoiding hypovolemia&#44; thus protecting from CIN&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">14</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Randomized trials with N-acetylcysteine had conflicting results but this drug can have a protective effect&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">15</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The authors tried to identify further markers of increased risk of AKI&#46; 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Editorial comment
Contrast-induced nephropathy: Can we better predict and prevent it?
Nefropatia induzida por contraste: poderemos prever e preveni-la melhor?
Pedro Pinto Cardosoa,b
a Structural and Coronary Heart Disease Unit, Centro Cardiovascular da Universidade de Lisboa, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal
b Serviço de Cardiologia, Departamento de Coração e Vasos, CHULN Hospital de Santa Maria, Lisboa, Portugal
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Contrast-induced nephropathy &#40;CIN&#41; is a major concern in daily practice for everyone working in interventional cardiology&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The use of contrast agents has been growing due to the increasing number of procedures that use them&#44; such as&#58; structural heart therapies and primary angioplasty for ST-segment elevation myocardial infarction &#40;STEMI&#41;&#46; Contrast-induced nephropathy has a major impact on prognosis after primary percutaneous coronary intervention &#40;PCI&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1&#44;2</span></a> In this particular setting&#44; it is problematic due to the clinical instability of the patient and the impossibility of prevention in an emerging situation&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Contrast-induced nephropathy is a well-known cause of acute renal failure but the underlying mechanisms are yet to be fully understood&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The evidence is in favor of a combination of direct toxic effects on tubular epithelial cells and renal ischemia as the pathogenetic role&#46; The generation of reactive oxygen species&#44; which in turn scavenge nitric oxide&#44; further increases hypoxia&#46;<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">4&#44;5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Identified risk factors for CIN are the baseline renal function itself&#44; diabetes&#44; acute myocardial infarction&#44; shock and the volume of contrast medium administered during the procedure&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">4</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Among patients with STEMI&#44; the role of contrast agents has been questioned in acute kidney injury &#40;AKI&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> In this study&#44; Caspi et al&#46; concluded that the risk for AKI was similar among STEMI patients regardless of exposure to contrast material&#46; Independent predictors of AKI in patients who underwent primary PCI included age &#8805;70 years&#44; insulin-treated diabetes&#44; diuretic therapy&#44; previous infarction&#44; baseline estimated glomerular filtration rate&#44; and variables related to the presence of pump failure &#40;higher Killip class&#44; intra-aortic balloon pump use&#41; and reduced left ventricular ejection fraction but not contrast agent dose&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In this issue Fatih Aksoy et al&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> assessed the association between total oxidant status &#40;TOS&#41;&#44; total antioxidant capacity &#40;TAC&#41; and CIN in patients with STEMI&#46; They assessed a cohort of 341 patients&#46; In a multivariate regression analysis&#44; they concluded that high-sensitivity C-reactive protein&#44; uric acid and oxidative status index predicted the development of CIN&#46; They also suggest that incorporating these variables into existing risk scores like the Mehran risk score<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">8</span></a> could improve its accuracy&#46; Nevertheless&#44; only 16&#46;7&#37; of these patients developed CIN&#44; which the authors acknowledged could have influenced their results&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The results suggest&#44; nonetheless&#44; that TOC&#44; TAC and oxidative stress index are associated with the development of CIN&#44; reinforcing the possibility that oxidative stress may be partially responsible for the development of CIN&#44; as already suggested by others&#46;<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9&#44;10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Preventive measures for CIN&#44; such as fluid administration&#44; pharmacological strategies&#44; use of different contrast agents and renal replacement therapies&#44; have been extensively assessed in many trials&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">There seems to be some consensus on fluid administration as a means of protecting from CIN&#44; but the results from trials are conflicting&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">11&#44;12</span></a> The addition of sodium bicarbonate may provide additional kidney protection by alkalinizing renal tubular fluid and thereby minimizing tubular damage&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">13</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Fluid administration possibly associated with furosemide forced diuresis seems to be a good strategy&#44; although there is the risk of hypovolemia&#46; The fear of giving too much volume&#44; mainly in patients with low ejection fraction can&#44; on the other hand&#44; lead to suboptimal protection&#46; Renal Guard&#44; a device enabling volume administration to be balanced with urine output&#44; showed that a high urine output was achievable&#44; while avoiding hypovolemia&#44; thus protecting from CIN&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">14</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Randomized trials with N-acetylcysteine had conflicting results but this drug can have a protective effect&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">15</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The authors tried to identify further markers of increased risk of AKI&#46; Still&#44; measuring TOC and TAC in daily practice does not seem feasible&#46; The result of this study may however contribute to further investigation on the mechanisms of CIN and possibly lead to novel therapeutic options to prevent CIN&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Currently&#44; hydration and possibly sodium bicarbonate&#47;N-acetylcysteine seem to be the best and only way to prevent CIN&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0080" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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