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Influencia de las sustancias diuréticas" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "334" "paginaFinal" => "336" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Severe arrhythmia due to hypokalemia. Influence from diuretic substances" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figura 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2116 "Ancho" => 3000 "Tamanyo" => 1004760 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Taquicardia ventricular polimorfa. Taquicardia ventricular polimorfa. QT aumentado.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Laura Salanova-Villanueva, Carmen Bernis-Carro, Luis Alberto-Blazquez, Jose Antonio Sanchez-Tomero" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Laura" "apellidos" => "Salanova-Villanueva" ] 1 => array:2 [ "nombre" => "Carmen" "apellidos" => "Bernis-Carro" ] 2 => array:2 [ "nombre" => "Luis" "apellidos" => "Alberto-Blazquez" ] 3 => array:2 [ "nombre" => "Jose Antonio" "apellidos" => "Sanchez-Tomero" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2013251415000279" "doi" => "10.1016/j.nefroe.2015.06.008" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251415000279?idApp=UINPBA000064" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0211699515000144?idApp=UINPBA000064" "url" => "/02116995/0000003500000003/v3_201512200017/S0211699515000144/v3_201512200017/es/main.assets" ] ] "itemSiguiente" => array:20 [ "pii" => "S2013251415000395" "issn" => "20132514" "doi" => "10.1016/j.nefroe.2015.07.001" "estado" => "S300" "fechaPublicacion" => "2015-05-01" "aid" => "20" "copyright" => "The Authors" "documento" => "simple-article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "cor" "cita" => "Nefrologia (English Version). 2015;35:337-9" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 5221 "formatos" => array:3 [ "EPUB" => 283 "HTML" => 4355 "PDF" => 583 ] ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letter to the Editor – Brief Case Reports</span>" "titulo" => "Subcapsular liver hematoma as a complication of an atypical hemolytic uremic syndrome" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "337" "paginaFinal" => "339" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Hematoma subcapsular hepático como complicación de síndrome hemolítico urémico atípico" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1099 "Ancho" => 2918 "Tamanyo" => 213047 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Abdominal computed tomography (A) and liver ultrasound (B) revealing a large subcapsular liver hematoma (13.8<span class="elsevierStyleHsp" style=""></span>cm<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>3.9<span class="elsevierStyleHsp" style=""></span>cm) (arrows) causing compression of the underlying liver parenchyma. No source for the hemorrhage was evident.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Emanuel Ferreira, Nuno Oliveira, Maria Marques, Helena Pinto, Ana Santos, Armando Carreira, Mário Campos" "autores" => array:7 [ 0 => array:2 [ "nombre" => "Emanuel" "apellidos" => "Ferreira" ] 1 => array:2 [ "nombre" => "Nuno" "apellidos" => "Oliveira" ] 2 => array:2 [ "nombre" => "Maria" "apellidos" => "Marques" ] 3 => array:2 [ "nombre" => "Helena" "apellidos" => "Pinto" ] 4 => array:2 [ "nombre" => "Ana" "apellidos" => "Santos" ] 5 => array:2 [ "nombre" => "Armando" "apellidos" => "Carreira" ] 6 => array:2 [ "nombre" => "Mário" "apellidos" => "Campos" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S0211699515000211" "doi" => "10.1016/j.nefro.2015.03.003" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0211699515000211?idApp=UINPBA000064" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251415000395?idApp=UINPBA000064" "url" => "/20132514/0000003500000003/v4_201511060045/S2013251415000395/v4_201511060045/en/main.assets" ] "itemAnterior" => array:20 [ "pii" => "S2013251415000280" "issn" => "20132514" "doi" => "10.1016/j.nefroe.2015.06.009" "estado" => "S300" "fechaPublicacion" => "2015-05-01" "aid" => "31" "copyright" => "The Authors" "documento" => "simple-article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "cor" "cita" => "Nefrologia (English Version). 2015;35:331-4" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 7013 "formatos" => array:3 [ "EPUB" => 284 "HTML" => 5917 "PDF" => 812 ] ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letters to the Editor – Brief Case Reports</span>" "titulo" => "Grover's disease in chronic kidney failure" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "331" "paginaFinal" => "334" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Enfermedad de Grover en fracaso renal crónico" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 732 "Ancho" => 1950 "Tamanyo" => 312144 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">(a) Aspect of the skin lesions: non-confluent brownish keratotic papules. (b) Areas of focal acantholysis with dyskeratosis (H&E, 200×).</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Laura Rodríguez-Pazos, Alejandro Vilas-Sueiro, Daniel González-Vilas, Cristina Durana" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Laura" "apellidos" => "Rodríguez-Pazos" ] 1 => array:2 [ "nombre" => "Alejandro" "apellidos" => "Vilas-Sueiro" ] 2 => array:2 [ "nombre" => "Daniel" "apellidos" => "González-Vilas" ] 3 => array:2 [ "nombre" => "Cristina" "apellidos" => "Durana" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0211699515000156" "doi" => "10.1016/j.nefro.2015.05.009" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0211699515000156?idApp=UINPBA000064" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251415000280?idApp=UINPBA000064" "url" => "/20132514/0000003500000003/v4_201511060045/S2013251415000280/v4_201511060045/en/main.assets" ] "en" => array:16 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letters to the Editor – Brief Case Reports</span>" "titulo" => "Severe arrhythmia due to hypokalemia. Influence from diuretic substances" "tieneTextoCompleto" => true "saludo" => "Dear Editor," "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "334" "paginaFinal" => "336" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Laura Salanova-Villanueva, Carmen Bernis-Carro, Luis Alberto-Blazquez, Jose Antonio Sanchez-Tomero" "autores" => array:4 [ 0 => array:3 [ "nombre" => "Laura" "apellidos" => "Salanova-Villanueva" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "Carmen" "apellidos" => "Bernis-Carro" ] 2 => array:2 [ "nombre" => "Luis" "apellidos" => "Alberto-Blazquez" ] 3 => array:2 [ "nombre" => "Jose Antonio" "apellidos" => "Sanchez-Tomero" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Servicio de Nefrología, Hospital de La Princesa, Madrid, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Arritmia cardiaca grave por hipopotasemia. Influencia de las sustancias diuréticas" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1611 "Ancho" => 2333 "Tamanyo" => 384857 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Distal tubule. Action of aldosterone on distal tubule.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">This was a case of a 25-year-old woman with no known allergies or relevant medical history and no toxic habits. She is an attorney and drinks 500–750<span class="elsevierStyleHsp" style=""></span>ml of beverages containing taurine and 1<span class="elsevierStyleHsp" style=""></span>l of caffeinated soda per day due to stress. The following details were observed: height 170<span class="elsevierStyleHsp" style=""></span>cm, weight 58<span class="elsevierStyleHsp" style=""></span>kg and BMI 20. She was admitted to the hospital for headache and tachycardia during the last two days after she did some sports and coinciding with an increase in the consumption of a beverages containing taurine. She denied chest pain or dyspnoea. Had no vomiting or diarrhoea and had no change in diuresis. She did not consume herbal products, drugs, teas, diuretics, liquorice or alcohol. <span class="elsevierStyleItalic">Physical examine</span>: Conscious, oriented, blood pressure 108/86, heart rate 110 beats per minute. Afebrile. Anodyne cardiopulmonary auscultation. Rest of the examination was normal. <span class="elsevierStyleItalic">Blood test</span>: normal red cell count, no elevation of cardiac or hepatic enzymes and coagulation test without alterations; creatinine 1.04<span class="elsevierStyleHsp" style=""></span>mg/dL, urea 31<span class="elsevierStyleHsp" style=""></span>mg/dL, potassium 1.73<span class="elsevierStyleHsp" style=""></span>mEq/L, sodium 134<span class="elsevierStyleHsp" style=""></span>mEq/L, magnesium 2.2<span class="elsevierStyleHsp" style=""></span>mg/dL, chloride 85<span class="elsevierStyleHsp" style=""></span>mEq/L, Albumin 4<span class="elsevierStyleHsp" style=""></span>g/dL. Arterial blood gas: Ph 7.580, PCO<span class="elsevierStyleInf">2</span> 46<span class="elsevierStyleHsp" style=""></span>mmHg, PO<span class="elsevierStyleInf">2</span> 86<span class="elsevierStyleHsp" style=""></span>mmHg, bicarbonate 43.1<span class="elsevierStyleHsp" style=""></span>mmol/L. Plasma anion gap (AG): 5.9<span class="elsevierStyleHsp" style=""></span>mEq/L. Urine: chloride 22.2<span class="elsevierStyleHsp" style=""></span>mEq/L, potassium 68.28<span class="elsevierStyleHsp" style=""></span>mEq/L, sodium 210<span class="elsevierStyleHsp" style=""></span>mmol/L, urea 920<span class="elsevierStyleHsp" style=""></span>mg/dL, creatinine 192.72<span class="elsevierStyleHsp" style=""></span>mg/dL, glucose 15<span class="elsevierStyleHsp" style=""></span>mg/dL. Urine anion gap: 256<span class="elsevierStyleHsp" style=""></span>mEq/L. Plasma osmolality: 278.2<span class="elsevierStyleHsp" style=""></span>mOsm/L. Urine osmolality: 573.3<span class="elsevierStyleHsp" style=""></span>mOsm/l. Transtubular potassium gradient: 15. Cortisol at 8<span class="elsevierStyleHsp" style=""></span>am and aldosterone in supine position were within the normal range. No alterations in urinary sediment. ECG: sinus rhythm, markedly enlarged QT (580<span class="elsevierStyleHsp" style=""></span>ms; corrected 700<span class="elsevierStyleHsp" style=""></span>ms); with frequent polymorphic ventricular tachycardia (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). An infusion of CLK was initiated via central line: 80<span class="elsevierStyleHsp" style=""></span>mEq within two hours and maintained with an infusion of 120<span class="elsevierStyleHsp" style=""></span>mEq/day. After 18<span class="elsevierStyleHsp" style=""></span>h, urine test was: sodium 25.3<span class="elsevierStyleHsp" style=""></span>mEq/L, potassium 6.2<span class="elsevierStyleHsp" style=""></span>mEq/L; in serum: sodium 142<span class="elsevierStyleHsp" style=""></span>mEq/L, potassium 2.8<span class="elsevierStyleHsp" style=""></span>mEq/L transtubular potassium gradient: 4. Venous blood gas: Ph 7.380, PCO<span class="elsevierStyleInf">2</span> 52<span class="elsevierStyleHsp" style=""></span>mmHg, HCO<span class="elsevierStyleInf">3</span> 30.8. Blood test at discharge: sodium 143<span class="elsevierStyleHsp" style=""></span>mEq/L, potassium 4.84<span class="elsevierStyleHsp" style=""></span>mEq/L, chloride 105<span class="elsevierStyleHsp" style=""></span>m Eq/L, pH 7.380, pCO<span class="elsevierStyleInf">2</span> 49<span class="elsevierStyleHsp" style=""></span>mmHg, bicarbonate 29<span class="elsevierStyleHsp" style=""></span>mmol/L. Urine: potassium 11.59<span class="elsevierStyleHsp" style=""></span>mmol/L, sodium 89<span class="elsevierStyleHsp" style=""></span>mmol/L, creatinine 266.27<span class="elsevierStyleHsp" style=""></span>mg/dL, urea 642<span class="elsevierStyleHsp" style=""></span>mg/dL. The ECG was normal. The evolution of ions in the urine suggested the presence of a diuretic substance that was suspended at admission. <span class="elsevierStyleItalic">Diagnoses</span>: hypokalaemia due to diuretic substances: taurine and caffeine, but not being able to rule out the presence of other diuretics, aggravated by the increase of insensitive losses and alkalemic state. A Bartter vs Gitelman-type tubulopathy was ruled out given the evolution of the ions in urine and the hormonal axis normality. Alteration in heart conduction due to hypokalaemia. Mixed alkalaemia: Chloride-resistant metabolic alkalosis due to diuretic substances and reactive respiratory alkalosis.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0010" class="elsevierStylePara elsevierViewall">Ninety percent of the potassium filtered at glomerular level is reabsorbed in the proximal tube. The distal tubule, by effect of the aldosterone, regulates the urinary output according to the body needs (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). Distal excretion of Kis modified by the amount of fluid, distal contribution of sodium, mineral corticoids and excretion of non-reabsorbable anions. The most common cause of hypokalaemia due to renal losses are non-potassium-sparing and similar diuretics. Hereditary tubulopathies (Bartter and Gitelman) may not be distinguishable from the intake of diuretics. Hyperaldosteronism and hypermineralcorticoidism cause hypokalaemia due to their action on the distal nephron. Potassium is a predominant intracellular cation. The best marker to assess the renal management of potassium is TTKG in euvolemia that assesses the mineralocorticoid action on the distal nephron: values <4 indicates absence and >7 presence of activity. Blood pressure, extrarenal losses, acid-base state, urinary ions and urine and plasma AG have to be assessed. In the presence of metabolic alkalosis, as in our case, chloride concentration decreases in order to compensate for the elevation of bicarbonate and the AG increases in proportion to the alkalosis severity, due to the lactate and the concentration of more anionic serum proteins. In turn, the kidney tends to increase the excretion of bicarbonate at proximal and distal tube level where there is a Cl<span class="elsevierStyleSup">−</span>/HCO<span class="elsevierStyleInf">3</span> exchange in the beta-intercalated cells of the collecting tubule. Serious chloride, potassium or extracellular space depletion inhibits this exchange. Urine AG is an indicator of urinary acidification. Positive values indicate that renal acidification is intact. Treatment must be oral. The intravenous line is reserved for serious hypokalaemia (<span class="elsevierStyleItalic">K</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>2.5<span class="elsevierStyleHsp" style=""></span>mEq/l), arrhythmia, acute myocardial infarction or digitalisation.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Some characteristics of the energy drinks diuretic components:</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Caffeine</span><p id="par0020" class="elsevierStylePara elsevierViewall">Natural xanthine. Energy drinks have levels between 75 and 174<span class="elsevierStyleHsp" style=""></span>mg per serving, others exceed 500<span class="elsevierStyleHsp" style=""></span>mg.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a> This stimulates the central nervous system, cardiovascular system, and central respiratory system; it relaxes the smooth bronchial muscle and striated muscle, increases acid gastric secretion and renal blood fluid and has diuretic properties. Many of these effects are caused by antagonic action on adenosine receptors.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a> It is rapidly distributed through the organism and crosses the placental and blood–brain barrier. It has hepatic metabolism (cytochrome P-450). It is clinically used as a respiratory stimulant in newborns with apnoea of prematurity. The adverse effects include insomnia, agitation, headache and tachycardia at elevated doses.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a> The changes in blood pressure response are not conclusive.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">5</span></a> It can produce dependence syndrome.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">6</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Taurine</span><p id="par0025" class="elsevierStylePara elsevierViewall">Conditionally essential amino acid. Its deficit is associated with cardiomyopathy, retinal degeneration and failure to thrive.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">7</span></a> Metabolic actions include: bile acids conjugation, osmolar regulation, detoxification, membranes stabilisation and modification of cellular sodium and calcium levels. It has positive inotropic action and protects the cardiac membrane from the adverse effects of hyperglycaemia.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">7,8</span></a> Its renalprotective effect is caused by its antioxidant action by controlling the effects generated by TGF-B1 and type I and IV collagen.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a> It increases the glomerular filtration rate, reduces sodium tubular reabsorption, reduces urine protein and inhibits antidiuretic hormone production.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">8,9</span></a> Clinically, it has been used in hypercholesterolaemia, epilepsy, cardiopathy, retinal macular degeneration, Alzheimer's disease, cystic fibrosis and hepatic diseases.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">10</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Both of them increase natriuresis increasing the arrival of sodium at the distal tubule: activating aldosterone and producing the entry of cellular sodium and the exit of potassium to the tubular light causing hypokalaemia.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Most of the supplements contained in the energy drinks have concentrations below the amounts associated with adverse effects.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a> The association of heart conduction alterations is not clear with studies for and against them.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">11,12</span></a> The combination of these drinks with alcohol may cause arrhythmias in subjects prone to them.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a></p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Caffeine" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Taurine" ] 2 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Salanova-Villanueva L, Bernis-Carro C, Alberto-Blazquez L, Sanchez-Tomero JA. Arritmia cardiaca grave por hipopotasemia. Influencia de las sustancias diuréticas. Nefrologia. 2015;35:334–336.</p>" ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2118 "Ancho" => 3007 "Tamanyo" => 1406383 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Polymorphic ventricular tachycardia. Increased QT.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1611 "Ancho" => 2333 "Tamanyo" => 384857 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Distal tubule. 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