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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Algorithm for detection and aetiological diagnosis of hyperkalaemia&#46; ACE&#44; angiotensin-converting enzyme&#59; ARB&#44; angiotensin II receptor blocker&#59; NSAID&#44; non-steroid anti-inflammatory drug&#59; TTKG&#44; transtubular potassium gradient&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In the paediatric age group&#44; hyperkalaemia tends to be asymptomatic&#44; so serum potassium levels greater than 5&#46;5&#8239;mEq&#47;L should be verified and investigated&#44; as they may be indicative of potentially severe diseases&#44; as occurred in the case presented here&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The patient was a boy aged 5 years with a personal history of obesity and type 1 diabetes in whom a blood chemistry panel ordered during a check up revealed a serum potassium level of 6&#46;8&#8239;mEq&#47;L in absence of other electrolyte abnormalities&#46; A second test confirmed the finding of hyperkalaemia&#46; Previous blood tests have not found abnormal levels of this ion&#44; and the patient had been asymptomatic at all times&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The assessment was completed with measurement of the arterial blood pressure&#44; which yielded values in the normal range for age and sex&#46; The patient underwent an electrocardiogram that did not evince any abnormalities&#44; as well as venous blood gas analysis that revealed mild metabolic acidosis with a pH of 7&#46;29&#44; a carbon dioxide pressure &#40;pCO<span class="elsevierStyleInf">2</span>&#41; of 39&#46;3&#8239;mmHg&#44; a serum bicarbonate level of 18&#46;2&#8239;mEq&#47;L and an excess base of &#8211;2&#46;3&#8239;mmol&#47;L&#46; We measured basal levels of aldosterone&#44; renin&#44; cortisol and adrenocorticotropic hormone &#40;ACTH&#41;&#44; which were normal&#46; We expanded the work up with analysis of a urine sample to calculate the transtubular potassium gradient&#44; which was of 1&#46;8 &#40;normal range&#44; 4&#8211;7&#41;&#44; which suggested deficient renal secretion of this ion with preserved renal function and a high calcium&#47;creatinine ratio of 0&#46;4&#8239;mg&#47;mg &#40;normal range&#44; &#60;0&#46;2&#8239;mg&#47;mg&#41;&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Retaking the family history revealed that the father had a history of long-term high blood pressure&#44; muscle weakness&#44; calcium renal lithiasis and episodes of atrial fibrillation in the past decade&#46; Both the father and the paternal grandfather &#40;who had died of cancer&#41; had elevated potassium levels in multiple blood tests&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Since the family history and tests performed to date suggested a hereditary aetiology of hyperkalaemia&#44; we approached the illness as a possible case of pseudohypoaldosteronism type II and ordered genetic testing for this syndrome&#44; which confirmed the suspected diagnosis with the detection of a heterozygous change in the <span class="elsevierStyleItalic">KLHL3</span> gene in both the patient and his father&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Following the diagnosis of pseudohypoaldosteronism type II&#44; despite remaining completely asymptomatic&#44; the patient started treatment with oral hydrochlorothiazide at a dose of 1&#8239;mg&#47;kg&#47;day&#44; which achieved normalization of serum levels of potassium and renal calcium excretion&#44; with a favourable outcome thereafter&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In conclusion&#44; if a paediatric patient has elevated potassium levels in 2 or more consecutive blood tests without an apparent cause&#44; the clinician should initiate an aetiological diagnosis&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">As <a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a> shows&#44; to determine the aetiology of the hyperkalaemia&#44; that the work up of these patients should include a urine test to calculate the transtubular potassium gradient and blood tests to measure the glomerular filtration rate and levels of renin&#44; aldosterone&#44; cortisol and ACTH&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> If the transtubular potassium gradient is low &#40;&#60;4&#41; and the glomerular filtration rate is normal&#44; the decreased excretion of this ion by the kidney suggests a mineralocorticoid deficiency or resistance&#44;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;3</span></a> and therefore&#44; the presence of normal or slightly elevated levels of renin and aldosterone guides the diagnosis toward unresponsiveness or resistance to the action of aldosterone in target cells&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Pseudohypoaldosteronism type II&#44; also known as Gordon syndrome&#44; is a rare disease characterised by hyperkalaemia&#44; hypercalciuria and high blood pressure with preserved renal function and normal or slightly elevated levels of aldosterone and renin&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;3</span></a> More than 180 families affected by this disease have been reported to date&#44; with a mean age at diagnosis of 26&#8239;&#177;&#8239;14 years&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> It is produced by changes in the <span class="elsevierStyleItalic">WNK1</span>&#44; <span class="elsevierStyleItalic">WNK4</span>&#44; <span class="elsevierStyleItalic">CUL3</span> or <span class="elsevierStyleItalic">KLHL3</span> gene that affect the renal excretion of sodium and potassium&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> In most cases&#44; the pattern of inheritance is autosomal dominant&#44; although cases of autosomal recessive changes in the <span class="elsevierStyleItalic">KLHL3</span> gene have also been described&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#8211;5</span></a> Thiazide diuretics are the first-line treatment and usually achieve adequate control of blood pressure&#44; decreasing the risk of renal lithiasis by decreasing renal excretion of calcium&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Thus&#44; early diagnosis of pseudohypoaldosteronism type II allows early initiation of treatment&#44; which may modify the long-term outcomes of disease&#46;</p></span>"
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