Case report
Transient early-childhood hyperkalaemia without salt wasting, pathophysiological approach of three cases
Hiperpotasemia transitoria del lactante sin pérdida salina, enfoque fisiopatológico de tres casos
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] 1 => array:3 [ "nombre" => "Alejandro" "apellidos" => "Balestracci" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "Ismael" "apellidos" => "Toledo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 3 => array:3 [ "nombre" => "Sandra Mariel" "apellidos" => "Martin" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 4 => array:3 [ "nombre" => "Laura" "apellidos" => "Beaudoin" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 5 => array:3 [ "nombre" => "Luis Eugenio" "apellidos" => "Voyer" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Nephrology Unit, Hospital General de Niños Pedro de Elizalde, Ciudad Autónoma de Buenos Aires, Argentina" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Department of Pediatrics, Universidad de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Hiperpotasemia transitoria del lactante sin pérdida salina, enfoque fisiopatológico de tres casos" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">In a <span class="elsevierStyleItalic">Nephrology Forum</span> on renal tubular acidosis in 1981, McSherry talked about a group of 13 infants with a condition he called early-childhood hyperkalaemia.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> It was characterised by hyperkalaemia and hyperchloraemic metabolic acidosis (MA) due to decreased ammonium excretion and bicarbonate in urine. Their urine also had decreased or inappropriately normal fractional excretion (FE) of potassium (K<span class="elsevierStyleSup">+</span>) for the elevated serum K<span class="elsevierStyleSup">+</span> values and normal FE of sodium (Na<span class="elsevierStyleSup">+</span>), with elevated or inappropriately normal plasma aldosterone and renin activity. This syndrome was attributed to a probable maturational disorder in the number or function of mineralocorticoid receptors in the distal tubule, leading to resistance to the action of aldosterone in the distal nephron.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–3</span></a> However, this theory did not explain the absence of salt wasting in these patients.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> In 1986, Appiani et al. published for the first time the cases of five patients with early-childhood hyperkalaemia, but with a different phenotype, as unlike the previous cases, they did have urinary salt wasting.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> To our knowledge, no new cases have been reported since then. We now present three additional patients with the syndrome described by McSherry,<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> which we refer to throughout the manuscript as “transient early-childhood hyperkalaemia without salt wasting” (TECH without salt wasting) to differentiate it from the variant described by Appiani et al.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> We provide a new pathophysiological approach based on advances in our understanding of the channels and transporters that regulate aldosterone-mediated Na<span class="elsevierStyleSup">+</span> and K<span class="elsevierStyleSup">+</span> transport in the distal tubule.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Methods</span><p id="par0010" class="elsevierStylePara elsevierViewall">Blood gases were determined in arterialised capillary samples. The pH and pCO<span class="elsevierStyleInf">2</span> in blood and urine were determined by an ABL 520® analyser, while Na<span class="elsevierStyleSup">+</span> and K<span class="elsevierStyleSup">+</span> were measured with the ion-selective Radiometer®. Urine samples were collected by catheter and kept anaerobically in a sealed syringe until measurement of urinary pH, pCO<span class="elsevierStyleInf">2</span> and bicarbonate (HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−)</span> (pHu, pCO<span class="elsevierStyleInf">2</span>u and HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span>u, respectively). The HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span>u was calculated with the Henderson-Hasselbalch equation, using the solubility constant of pCO<span class="elsevierStyleInf">2</span> in blood (α<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>0.00301) and a blood pK of 6.1.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Urinary ammonia was inferred by the urine anion gap (AG), compared to spontaneous MA or during the furosemide test.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> The FE of Na<span class="elsevierStyleSup">+</span>, K<span class="elsevierStyleSup">+</span> and HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span> were calculated with the formula (U/P of the substance)/(U/P creatinine)<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>100; where U and P represent the concentrations in urine and plasma, respectively. Creatinine was determined with the Jaffé method, while plasma renin and aldosterone were measured by radioimmunoassay in samples collected at nine o'clock in the morning. Hyperchloraemia was defined as a chloride (Cl–) concentration >75% of the concentration of Na<span class="elsevierStyleSup">+</span>.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> The plasma AG was calculated with the formula Na<span class="elsevierStyleSup">+</span> – (Cl– + HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span>), considering a normal value 12<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>2, and the urinary AG with the formula (Na<span class="elsevierStyleSup">+</span> + K<span class="elsevierStyleSup">+</span>) – Cl<span class="elsevierStyleSup">−</span>, considering that any negative value suggests normal ammonium excretion, while any positive value reflects a decrease in excretion. The alkali loading test to determine the difference in blood and urine pCO<span class="elsevierStyleInf">2</span> (U-B pCO<span class="elsevierStyleInf">2</span>) was adapted for use in children and a difference ≥20<span class="elsevierStyleHsp" style=""></span>mmHg was considered normal.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Calciuria was determined in isolated urine, averaging three determinations, dividing the calcium concentration with the creatinine concentration and considering a normal value to be <0.8.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> The transtubular potassium gradient was calculated with the formula (U/P of K<span class="elsevierStyleSup">+</span>)/(U/P osmolality)<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>100; osmolality was measured with a vapour pressure osmometer (Wescor®), with the value in infants with hyperkalaemia expected to be >5.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The normal electrolyte and creatinine values were the usual ones for the age groups studied.<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9–12</span></a> Blood pressure was recorded with an oscillometric device. Three consecutive readings were made, we considered the value resulting from the average of the three measurements.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Patients</span><p id="par0015" class="elsevierStylePara elsevierViewall">Three patients (two male) aged 30, 45 and 120 days, respectively, hospitalised for bronchiolitis syndrome, had laboratory parameters compatible with TECH without salt wasting. Two of the patients had no history of perinatal problems, while the 120-day-old boy was born at 30 weeks' gestation with a weight of 1.735<span class="elsevierStyleHsp" style=""></span>kg (adequate weight for gestational age) and had had hyaline membrane disease requiring mechanical ventilation for seven days. During their hospital stay, sustained hyperkalaemia was found in all cases, accompanied by normal natraemia and hyperchloraemic MA. None of them was receiving medication or had any other external factors likely to cause elevation of serum K<span class="elsevierStyleSup">+</span>. Furthermore, the disorder persisted despite treatment with β2 agonists, indicated by the respiratory symptoms. All three patients had normal blood pressure: the 30-day-old 70/50<span class="elsevierStyleHsp" style=""></span>mmHg; the 45-day-old 75/55<span class="elsevierStyleHsp" style=""></span>mmHg; and the 120-day-old 70/50<span class="elsevierStyleHsp" style=""></span>mmHg. Blood AG, lactic acid, ammonium and creatinine values were normal in all patients. Plasma renin activity and serum aldosterone were inappropriately normal in all three cases. In addition, all three had low or inappropriately normal FEK<span class="elsevierStyleSup">+</span> for the degree of hyperkalaemia, with normal FENa<span class="elsevierStyleSup">+</span> (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). The transtubular potassium gradient was only determined in the 120-day-old patient and was 2.66. Calcium excretion was normal, with values of 0.66, 0.5 and 0.72 in the 30-, 45- and 120-day-old patient, respectively, and urinary infection was ruled out by negative urine culture. Renal ultrasounds were normal, with no findings compatible with urological disorders such as dilated urinary tract and/or bladder disease. Congenital adrenal hyperplasia was ruled out based on the finding of normal external genitalia along with normal serum levels of 17-OH progesterone, 18-OH corticosterone, ACTH, cortisol and dehydroepiandrosterone sulfate. The urinary AG was positive, becoming negative after administration of furosemide; while the FE HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span> was elevated after normalising blood values with alkalis (<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>). In addition, compromise of hydrogen (H<span class="elsevierStyleSup">+</span>) secretion through the distal tubule was ruled out as cause of the MA, as the U-B pCO<span class="elsevierStyleInf">2</span> was normal (>20<span class="elsevierStyleHsp" style=""></span>mmHg) (<a class="elsevierStyleCrossRef" href="#tbl0015">Table 3</a>).</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">The hyperkalaemia was treated with cation exchange resins 1<span class="elsevierStyleHsp" style=""></span>g/kg every 8−12<span class="elsevierStyleHsp" style=""></span>h and furosemide 1<span class="elsevierStyleHsp" style=""></span>mg/kg every 6<span class="elsevierStyleHsp" style=""></span>h. The furosemide was later replaced by hydrochlorothiazide, to prevent loop diuretic-related hypercalciuria. However, just recently we were able to normalise the serum concentration of K<span class="elsevierStyleSup">+</span>, and the MA, after the addition of sodium bicarbonate orally at 2<span class="elsevierStyleHsp" style=""></span>mEq/kg/day. During follow-up, treatment was suspended at times, but with reappearance of the metabolic disorders, until definitive resolution was verified at 6 months in the 30-day-old patient, 7 months in the 120-day-old and 11 months in the 45-day-old. Over the course of their recuperation, weight and height recovery was observed in all three cases. The 30-day-old patient weighed 3.6<span class="elsevierStyleHsp" style=""></span>kg (3rd–10th percentile) at diagnosis and measured 52<span class="elsevierStyleHsp" style=""></span>cm (10th percentile), reaching a weight of 7.9<span class="elsevierStyleHsp" style=""></span>kg and a height of 67<span class="elsevierStyleHsp" style=""></span>cm at six months of age, both in the 25th–50th percentile. In the case of the 45-day-old, who at the beginning weighed 3.6<span class="elsevierStyleHsp" style=""></span>kg and measured 50<span class="elsevierStyleHsp" style=""></span>cm, both below the 3rd percentile, by the age of 11 months weighed 9.4<span class="elsevierStyleHsp" style=""></span>kg (50th percentile) and measured 74<span class="elsevierStyleHsp" style=""></span>cm (25th–50th percentile). Similarly, the 120-day-old weighed 3.25<span class="elsevierStyleHsp" style=""></span>kg (3rd percentile) and measured 52<span class="elsevierStyleHsp" style=""></span>cm (3rd–10th percentile) at diagnosis, but had reached 5.5<span class="elsevierStyleHsp" style=""></span>kg and a height of 60<span class="elsevierStyleHsp" style=""></span>cm, both in the 25th–50th percentile, at the age of seven months.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Discussion</span><p id="par0025" class="elsevierStylePara elsevierViewall">In this study, we describe in detail three patients with TECH without salt wasting with a metabolic pattern similar to those discussed by McSherry.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Our patients had MA induced by the same hyperkalaemia, as it inhibits ammoniagenesis, leading to a decrease in the urinary excretion of ammonia.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> Moreover, the elevated K<span class="elsevierStyleSup">+</span> concentration was also responsible for the bicarbonate in urine which, although showing a lower level of excretion than that observed in proximal renal tubular acidosis (pRTA), was higher than that in healthy infants and children in whom HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span> secretion is negligible.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Therefore, persistent MA caused by the two mechanisms mentioned could have brought about the growth retardation observed in these children. H<span class="elsevierStyleSup">+</span> secretion by the cortical collecting duct (CCD) was adequate based on the fact that the U-B pCO<span class="elsevierStyleInf">2</span> was normal, this being the most sensitive marker in H<span class="elsevierStyleSup">+</span> secretion by the intercalated α cells, and so distal renal tubular acidosis (dRTA) could be ruled out. It is worth mentioning that while in cases caused by a gradient defect due to increased permeability of the luminal membrane of the CCD, as can occur in amphotericin toxicity, the U-B pCO<span class="elsevierStyleInf">2</span> is normal (≥20<span class="elsevierStyleHsp" style=""></span>mmHg) but the urinary pH remains higher than 5.5 compared to MA,<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> in our patients, the pH fell below 5.5, making it unlikely that this mechanism was responsible for their acidosis. We were able to differentiate our patients' conditions from pseudohypoaldosteronism type 1<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> or being secondary to urinary tract infection and/or malformations<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> by the absence of salt wasting from the kidney and hyponatraemia, and by the lack of ultrasound findings consistent with urinary disease and negative urine cultures. They can also be differentiated from the condition described by Spitzer-Weinstein, characterised by a pattern similar to Gordon's syndrome but without hypertension, due to the younger age of presentation, the need to combine sodium bicarbonate with thiazides to normalise the internal environment, and the transient nature of the condition.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Two patients had a marked decrease in FEK<span class="elsevierStyleSup">+</span> (1.9% and 3.2%); the patient in whom the transtubular potassium gradient was calculated consistently had a low value compatible with decreased FEK<span class="elsevierStyleSup">+</span>. In addition, it is worth mentioning that in the 45-day-old patient, despite having a normal value of 13.2%, the FEK<span class="elsevierStyleSup">+</span> was also considered inappropriate for his hyperkalaemia, as in situations of acute and chronic hyperkalaemia, FEK<span class="elsevierStyleSup">+</span> should increase dramatically.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">As we mentioned earlier, the pathophysiology of the patients reported by McSherry was attributed to a probable maturational disorder of the mineralocorticoid receptors of the distal tubule.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2</span></a> However, this theory does not explain the absence of salt wasting that would be expected along with K<span class="elsevierStyleSup">+</span> retention because aldosterone cannot adequately bind to its tubular receptor, as occurs in pseudohypoaldosteronism type 1 or secondary to urinary infection and/or urinary tract disease.<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,17</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Studies carried out in newborn mammals have observed an adequate number of receptors for aldosterone and of binding sites for the hormone-receptor complex at the nuclear level, so it is now thought that early hyposensitivity to aldosterone is a post-receptor phenomenon.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> This could explain the dissociation from the normal response to aldosterone observed in our patients, who abnormally retained K<span class="elsevierStyleSup">+</span> but continued to have adequate reabsorption of Na<span class="elsevierStyleSup">+</span>. In fact, in an early phase, once in the nucleus, the mineralocorticoid-receptor complex causes the activation and repression of genes capable of modulating the activity of the main Na<span class="elsevierStyleSup">+</span> and K<span class="elsevierStyleSup">+</span> transporters already in the distal tubular segments, especially the Na<span class="elsevierStyleSup">+</span>/K<span class="elsevierStyleSup">+</span> ATPase pump, the thiazide-sensitive Na<span class="elsevierStyleSup">+</span>/Cl– co-transporter (NCC) and the epithelial sodium channel (ENaC).<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> Among these early aldosterone-induced genes are also different kinases, including WNK4 (lysine-deficient kinases), Sgk-1 (serum- and glucocorticoid-regulated kinase 1), and those of the Src family of protein tyrosine kinases (SFKs).<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">20–24</span></a> Subsequently, in its late phase, aldosterone directly modulates the levels of expression of the different transporters of Na<span class="elsevierStyleSup">+</span> and K<span class="elsevierStyleSup">+</span>,<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> and so contributes to the reabsorption of Na<span class="elsevierStyleSup">+</span> by stimulating the Na<span class="elsevierStyleSup">+</span>/K<span class="elsevierStyleSup">+</span> ATPase pumps, the NCC and the ENaC; and also indirectly through intervention of Sgk-1, which stimulates ENaC and Na<span class="elsevierStyleSup">+</span>/K<span class="elsevierStyleSup">+</span> ATPase pump activity.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">20,22</span></a> In relation to the management of K<span class="elsevierStyleSup">+</span>, the action of aldosterone is produced by different kinases modulating the actions of the renal outer medullary potassium (ROMK) channels, which regulate cation efflux in the collecting tubule.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">20,21</span></a> WNK4 inhibits expression of ROMK channels, reducing the secretion of K<span class="elsevierStyleSup">+</span>, an action which is then reversed by Sgk1.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21,23,25</span></a> In addition, the inhibition of WNK4 by SgK1 is attenuated by the SFK in order to prevent K<span class="elsevierStyleSup">+</span> secretion in the absence of hyperkalaemia.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> This attenuation is also observed in hypovolaemia, in which there is an increase in aldosterone and SgK1 activity, leading to Na<span class="elsevierStyleSup">+</span> retention and increased K<span class="elsevierStyleSup">+</span> secretion. However, if concomitantly K<span class="elsevierStyleSup">+</span> influx is low, as previously mentioned, SFKs attenuate SgK1, whereby WNK4 restores ROMK inhibition, decreasing K<span class="elsevierStyleSup">+</span> secretion. In this situation we can see how the effects of aldosterone can become dissociated.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> Another situation where this dissociation is observed is in patients with Gordon's syndrome (pseudohypoaldosteronism type 2), in which inhibitory mechanisms other than mutated WNK4 on NCC and ROMK channels could explain the uncoupling. Nonsense mutations of these kinases cause loss of inhibition of NCC expression, generating Na<span class="elsevierStyleSup">+</span> retention and hypertension on the one hand and, on the other, increased inhibition of ROMK channels, which leads to hyperkalaemia.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Similarly, the lack of coordination between the complex mechanism of regulation and counter-regulation of kinases, especially WNK4 as a multifunctional regulator that can dissociate the effects of aldosterone on Na<span class="elsevierStyleSup">+</span> and K<span class="elsevierStyleSup">+</span> secretion, could be responsible for what we observed in our patients, who reabsorbed Na<span class="elsevierStyleSup">+</span> normally but had decreased K<span class="elsevierStyleSup">+</span> secretion. This could represent the accentuation of a necessary physiological process in newborns and infants in the first few months, as they need a positive balance of K<span class="elsevierStyleSup">+</span> and Na<span class="elsevierStyleSup">+</span> to cope with the rapid somatic growth they undergo. This is essentially achieved thanks to retention of these electrolytes by the CCD, as a result of which they also have higher serum K<span class="elsevierStyleSup">+</span> levels than older infants and children.<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">25,27,28</span></a> Furthermore, as shown in animal models, in the first three weeks of postnatal life there is a lack of expression of the ROMK channel protein from the principal cells of the CCD, with K<span class="elsevierStyleSup">+</span> excretion only reaching levels comparable to those of an adult at six weeks of life.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> Along the same lines, the Maxi K<span class="elsevierStyleSup">+</span> channel, which is the other channel involved in K<span class="elsevierStyleSup">+</span> secretion in CCD, particularly in response to increased distal tubular flow, is only expressed after four weeks of postnatal life,<a class="elsevierStyleCrossRefs" href="#bib0145"><span class="elsevierStyleSup">29,30</span></a> so it could be another contributing factor to hyperkalaemia. These observations would also explain the fact that it is a transient tubular disorder, as occurred in our patients.</p><p id="par0045" class="elsevierStylePara elsevierViewall">In conclusion, the evidence suggests that TECH without salt wasting may be the exaggerated expression of a maturational phenomenon, characterised by a later expression of the channels that regulate K<span class="elsevierStyleSup">+</span> balance in the CCD under the influence of aldosterone, whose maturation is normally slow, in order to ensure the high K<span class="elsevierStyleSup">+</span> retention necessary for rapid somatic growth. As it is a transient condition with few clinical manifestations, it should be considered among the causes of hyperkalaemia and growth retardation in the first months of life.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflicts of interest</span><p id="par0050" class="elsevierStylePara elsevierViewall">Nothing to declare.</p><p id="par0055" class="elsevierStylePara elsevierViewall">This study received no specific funding from public, private or non-profit organisations.</p><p id="par0060" class="elsevierStylePara elsevierViewall">This study was approved by the ethics committee at our institution.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres1733794" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1529817" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1733795" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1529816" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Methods" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Patients" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Discussion" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Conflicts of interest" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2020-07-31" "fechaAceptado" => "2020-12-16" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1529817" "palabras" => array:4 [ 0 => "Transient early-childhood hyperkalemia without salt wasting" 1 => "Hyperkalemia" 2 => "Hyperchloremic metabolic acidosis" 3 => "Aldosterone" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1529816" "palabras" => array:4 [ 0 => "Hiperpotasemia transitoria del lactante sin pérdida salina" 1 => "Hiperpotasemia" 2 => "Acidosis metabólica hiperclorémica" 3 => "Aldosterona" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Two types of early childhood hyperkalemia had been recognized, according to the presence or absence of urinary salt wasting. This condition was attributed to a maturation disorder of aldosterone receptors and is characterized by sustained hyperkalemia, hyperchloremic metabolic acidosis (MA) due to reduced ammonium urinary excretion and bicarbonate loss, and normal creatinine with growth delay. We present 3 patients of the type without salt wasting, which we will call <span class="elsevierStyleItalic">transient early-childhood hyperkalemia (TECHH) without salt wasting</span>, and discuss its physiopathology according to new insights into sodium and potassium handling by the aldosterone in distal nephron. In 3 children from 30 to 120-day-old admitted with bronchiolitis and growth delay hyperkalemia was found in routine laboratory. Further studies revealed a normal creatinine with inappropriately normal or low fractional excretion (FE) of potassium, accompanied by inadequately normal serum aldosterone and plasma renin activity for their higher plasma potassium levels, but without urine salt wasting. They also presented hyperchloremic MA with FE of bicarbonate 0.58%–2.2%, positive urinary anion gap during MA and normal ability to acidify the urine. Based on these findings a diagnosis of TECHH without salt wasting was made and they were treated sodium bicarbonate and hydrochlorothiazide with favorable response. The condition was transient in all cases leading to treatment discontinuation. Given that TECCH without salt wasting is a tubular disorder of transient nature with mild symptoms; it must be keep in mind in the differential diagnosis of hyperkalemia in young children.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Se reconocen dos variedades de hiperpotasemia temprana de la infancia (del inglés <span class="elsevierStyleItalic">Early childhood hyperkalemia</span>) según la presencia o no de pérdida salina urinaria. Se trata de una entidad atribuida a un desorden madurativo en los receptores de aldosterona caracterizada por hiperpotasemia, acidosis metabólica (AM) hiperclorémica por diminución de la eliminación de amonio y bicarbonaturia, y creatinina normal con retraso de crecimiento. Presentamos 3 pacientes de la forma con ausencia de pérdida salina, a la que denominaremos <span class="elsevierStyleItalic">hiperpotasemia transitoria del lactante (HTL) sin pérdida salina</span>, y discutimos su fisiopatología en relación a los nuevos conocimientos en el manejo tubular del sodio y el potasio por la aldosterona. En 3 pacientes de entre 30 y 120 días de edad con bronquiolitis y retraso de crecimiento se encontró hiperpotasemia en laboratorio de rutina. Presentaban creatinina normal, excreción fraccionada (EF) de potasio disminuida o inapropiadamente normal junto a niveles de aldosterona y renina plasmática inadecuadamente normales para el estado de hiperpotasemia, pero sin pérdida salina. También cursaban con AM hiperclorémica con bicarbonaturia (EF bicarbonato 0,58%–2,2%), anión restante urinario positivo durante AM y capacidad normal para acidificar la orina. En base a estos hallazgos se diagnosticó HTL sin pérdida salina y se trataron con bicarbonato de sodio e hidroclorotiazida con buena respuesta. El cuadro fue transitorio permitiendo la suspensión del tratamiento. Dado que el HTL sin pérdida salina es un desorden tubular transitorio con síntomas leves debe tenerse presente en el diagnóstico diferencial de hiperpotasemia en niños pequeños.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0020">Please cite this article as: Alvarado C, Balestracci A, Toledo I, Martin SM, Beaudoin L, Voyer LE. Hiperpotasemia transitoria del lactante sin pérdida salina, enfoque fisiopatológico de tres casos. Nefrologia. 2022;42:203–208.</p>" ] ] "multimedia" => array:3 [ 0 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0025" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:3 [ "leyenda" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">AG: anion gap; FE: fractional excretion; PRA: plasma renin activity; U-B pCO<span class="elsevierStyleInf">2</span>: difference in blood and urine pCO<span class="elsevierStyleInf">2</span>.</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">The normal values for age are shown in brackets.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " rowspan="2" align="left" valign="middle" scope="col">Age (days)</th><th class="td-with-role" title="\n \t\t\t\t\ttable-head\n \t\t\t\t ; entry_with_role_colgroup " colspan="8" align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Plasma</th><th class="td-with-role" title="\n \t\t\t\t\ttable-head\n \t\t\t\t ; entry_with_role_colgroup " colspan="6" align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Urine</th></tr><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Creatinine <a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a> mg/dl (0.5<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>0.2) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Aldosterone pg/mL (300−916) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">PRA ng/mL/h (14.6−48.2) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">K<span class="elsevierStyleSup">+</span> mEq/l (3.5−5.5) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Na<span class="elsevierStyleSup">+</span> mEq/l (135−145) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">HCO<span class="elsevierStyleInf">3</span>– mEq/l (24<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>4) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Cl<span class="elsevierStyleSup">−</span>mEq/l (98−106) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">AG mEq/l (12<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>4) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">FEK<span class="elsevierStyleSup">+</span> % (5−12) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">FENa<span class="elsevierStyleSup">+</span> % (0.4−0.8) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">FEHCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span> % (Negligible) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pCO<span class="elsevierStyleInf">2</span> U-B mmHg (≥20) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pH <a class="elsevierStyleCrossRef" href="#tblfn0010"><span class="elsevierStyleSup">b</span></a> (<5.5) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">AG mEq/l (+) <a class="elsevierStyleCrossRef" href="#tblfn0015"><span class="elsevierStyleSup">c</span></a> \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">45 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.52 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">400 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">18 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6.45 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">140 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">18.55 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">114 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.45 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">13.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.3 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.74 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">23 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+34 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">120 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.25 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">322 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">26.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">138 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">17.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">114 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">3.20 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.60 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.58 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">22 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+21 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">30 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.25 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">460 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">19 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">137 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">13.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">110 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">13.9 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.9 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.15 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">2.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">21 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+6.6 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2940480.png" ] ] ] "notaPie" => array:3 [ 0 => array:3 [ "identificador" => "tblfn0005" "etiqueta" => "a" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Determined with the Jaffé method.</p>" ] 1 => array:3 [ "identificador" => "tblfn0010" "etiqueta" => "b" "nota" => "<p class="elsevierStyleNotepara" id="npar0010">Any positive value in acidosis is abnormal.</p>" ] 2 => array:3 [ "identificador" => "tblfn0015" "etiqueta" => "c" "nota" => "<p class="elsevierStyleNotepara" id="npar0015">Urine pH measured in isolated sample.</p>" ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Metabolic profile in three patients with transient early-childhood hyperkalaemia without salt wasting.</p>" ] ] 1 => array:8 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0030" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Values after administration of alkali loading.</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">s Determination in serum.</p><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">u Determination in urine.</p>" "tablatextoimagen" => array:1 [ 0 => array:1 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Age (days) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span>s mEq/l \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pHu \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pCO<span class="elsevierStyleInf">2</span>u mmHg \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span>u mEq/l \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">FE HCO<span class="elsevierStyleInf">3</span>– % \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">30 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">21 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.15 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">40 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">15 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">2.2 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">45 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">23.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">46.7 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">12.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.74 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">120 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">22 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">30 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">11 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">0.58 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Determination of bicarbonate and fractional bicarbonate excretion in three patients with transient early-childhood hyperkalaemia without salt wasting.</p>" ] ] 2 => array:8 [ "identificador" => "tbl0015" "etiqueta" => "Table 3" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0035" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Values after administration of alkali loading.</p><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">s Determination in serum.</p><p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">u Determination in urine.</p>" "tablatextoimagen" => array:1 [ 0 => array:1 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Age (days) \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pHu \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pCO<span class="elsevierStyleInf">2</span>u mmHg \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">−</span>u mEq/l \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">pCO<span class="elsevierStyleInf">2</span> u-s mmHg \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">30 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.48 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">55 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">39 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">21 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">45 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.50 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">60 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">45 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">23 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">120 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">7.49 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">67 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">40 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">22 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Alkali loading test to determine the difference between urine and blood pCO<span class="elsevierStyleInf">2</span> (U-B pCO<span class="elsevierStyleInf">2</span>) in three patients with transient early-childhood hyperkalaemia without salt wasting.</p>" ] ] ] "bibliografia" => array:2 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 4 | 9 | 13 |
| 2024 October | 54 | 50 | 104 |
| 2024 September | 71 | 26 | 97 |
| 2024 August | 71 | 51 | 122 |
| 2024 July | 46 | 26 | 72 |
| 2024 June | 71 | 59 | 130 |
| 2024 May | 66 | 41 | 107 |
| 2024 April | 71 | 39 | 110 |
| 2024 March | 59 | 43 | 102 |
| 2024 February | 58 | 53 | 111 |
| 2024 January | 43 | 31 | 74 |
| 2023 December | 49 | 25 | 74 |
| 2023 November | 60 | 50 | 110 |
| 2023 October | 38 | 73 | 111 |
| 2023 September | 30 | 99 | 129 |
| 2023 August | 41 | 29 | 70 |
| 2023 July | 58 | 32 | 90 |
| 2023 June | 49 | 30 | 79 |
| 2023 May | 58 | 42 | 100 |
| 2023 April | 38 | 34 | 72 |
| 2023 March | 59 | 23 | 82 |
| 2023 February | 47 | 31 | 78 |
| 2023 January | 41 | 45 | 86 |
| 2022 December | 84 | 45 | 129 |
| 2022 November | 55 | 60 | 115 |
| 2022 October | 81 | 85 | 166 |
| 2022 September | 57 | 56 | 113 |
| 2022 August | 55 | 42 | 97 |
| 2022 July | 60 | 56 | 116 |
| 2022 June | 73 | 52 | 125 |
| 2022 May | 51 | 54 | 105 |
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