Response to the comment on: Cardiac troponin I and creatine kinase MB isoenzyme in patients with chronic renal failure
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Flores-Solís, Juan L. Hernández-Domínguez, Alfonso Otero-González, José R. González-Juanatey" "autores" => array:4 [ 0 => array:4 [ "nombre" => "Larry M." "apellidos" => "Flores-Solís" "email" => array:1 [ 0 => "lmlab7@yahoo.es" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "nombre" => "Juan L." "apellidos" => "Hernández-Domínguez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:3 [ "nombre" => "Alfonso" "apellidos" => "Otero-González" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] 3 => array:3 [ "nombre" => "José R." "apellidos" => "González-Juanatey" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "affc" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Laboratorio de Análisis Clínicos, Complejo Hospitalario de Ourense, " "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] 1 => array:3 [ "entidad" => "Servicio de Nefrología, Complejo Hospitalario de Ourense, " "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] 2 => array:3 [ "entidad" => "Servicio de Cardiología, Complejo Hospitalario Universitario de Santiago de Compostela, " "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "affc" ] ] ] ] "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor:</span></p><p class="elsevierStylePara">We are grateful for the comments and interest of Dr Cakar M. and his collaborators regarding our study entitled “Cardiac troponin I and creatine kinase MB isoenzyme in patients with chronic renal failure” in which we included 484 consecutive chronic renal failure (CRF) patients with suspected acute coronary syndrome (ACS). Due to CRF patients being a high cardiovascular risk population, we decided to apply a strategy to improve diagnostic sensitivity and we obtained a cardiac troponin I (cTnI) cut-off value that was significantly different from that used for the general population to diagnose ACS, although it had been reported that by decreasing the 99<span class="elsevierStyleSup">th</span> percentile of cTnI (cut-off value), more patients with ACS<span class="elsevierStyleSup">1 </span>at risk of recurrent myocardial infarction (MI) or death would be identified, but the diagnosis of MI would increase by 47%.<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara">Moreover, it is important to know that any cardiac damage may cause the release of troponins from myocytes as complexes or as free troponin in circulation and there are many causes of increased troponins that are not related to ACS, among which are: 1) cardiac causes (congestive heart failure, tachycardia, left ventricular hypertrophy, myocardial contusion, myocarditis, pericarditis, cardiac amyloidosis, heart surgery, cardioversion, percutaneous coronary intervention, coronary vasospasm, radiofrequency ablation, other), 2) non-cardiac causes (chronic renal failure, sepsis, stroke, pulmonary embolism, primary pulmonary hypertension, critically ill patients, chemotherapy, sympathomimetic agents, intense resistance exercise, other) and 3) methodological causes (fibrin, haemolysis, heterophile antibodies, rheumatoid factor, other).<span class="elsevierStyleSup">3,4</span></p><p class="elsevierStylePara">In patients with CRF, the mechanisms that may explain the nonspecific increases in cTnI are mainly further heart damage and decreased kidney function.<span class="elsevierStyleSup">5</span> In our study, the main causes of increased cTnI in the Other Cardiac Pathologies (OCP) group were congestive heart failure, atrial fibrillation and tachycardia, while in the Other Non-cardiac Pathologies (ONCP) group they were high blood pressure, stroke and pneumonia, but we believe that all the causes described should be taken into consideration as potential confounding factors whenever high cTnI concentrations are found in patients with CRF and an absence of ACS.</p><p class="elsevierStylePara"> </p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article.</p>" "pdfFichero" => "P1-E562-S4416-A12321-EN.pdf" "tienePdf" => true "tieneResumen" => true "resumen" => array:1 [ "en" => array:1 [ "resumen" => "<p class="elsevierStylePara">Response to Cakar M.</p> <p class="elsevierStylePara">Comment in Nefrologia 2013;33(6):852</p> <p class="elsevierStylePara">Nefrologia 2012;32(6):809-18.</p> <p class="elsevierStylePara">PMID: 23169364 [PubMed - in process]</p>" ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF task force for the redefinition of myocardial infarction. Universal definition of myocardial infarction. J Am Coll Cardiol 2007;50:2173-95. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18036459" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 1 => array:3 [ "identificador" => "bib2" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Mills NL, Lee KK, McAllister DA, Churchhouse A, MacLeod M, Stoddart M, et al. Implications of lowering threshold of plasma troponin concentration in diagnosis of myocardial infarction: cohort study. BMJ 2012;344:e1533. <a href="http://www.ncbi.nlm.nih.gov/pubmed/22740569" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 2 => array:3 [ "identificador" => "bib3" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Agewell S, Giannitsis E, Jernberg T, Katus H. Troponin elevation in coronary vs non-coronary disease. Eur Heart J 2011;32:404-11. <a href="http://www.ncbi.nlm.nih.gov/pubmed/21169615" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 3 => array:3 [ "identificador" => "bib4" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Jaffe AS, Ordonez-Llanos J. Troponinas ultrasensibles en el dolor torácico y los síndromes coronarios agudos. ¿Un paso hacia adelante? Rev Esp Cardiol 2010;63:763-9." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 4 => array:3 [ "identificador" => "bib5" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "deFilippi C, Seliger SL, Kelley W, Duh SH, Hise M, Christenson RH, et al. Interpreting cardiac troponin results from high-sensitivity assays in chronic renal disease without acute coronary syndrome. Clin Chem 2012;58:1342-51. <a href="http://www.ncbi.nlm.nih.gov/pubmed/22791885" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/20132514/0000003300000006/v0_201502091623/X2013251413053288/v0_201502091624/en/main.assets" "Apartado" => array:4 [ "identificador" => "35439" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor - Comments on published articles" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/20132514/0000003300000006/v0_201502091623/X2013251413053288/v0_201502091624/en/P1-E562-S4416-A12321-EN.pdf?idApp=UINPBA000064&text.app=https://revistanefrologia.com/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X2013251413053288?idApp=UINPBA000064" ]
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