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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#44;</span></p><p class="elsevierStylePara">Hypokalemia is one of the most common electrolyte abnormalities which etiology can be unclear and the incorrect diagnosis can result in the wrong treatment&#46;</p><p class="elsevierStylePara">Gitelman syndrome &#40;GS&#41; is an autosomal recessive disorder of the thiazide-sensitive sodium chloride cotransporter&#44; expressed at the distal convoluted tubule &#40;DCT&#41;&#46; The mutation is found in the <span class="elsevierStyleItalic">SLC12A3 </span>gene&#44; but there are also others&#46; Its prevalence is estimated to range 25 cases per 1 million&#46;<span class="elsevierStyleSup">1</span> Acquired GS is rarer and usually associated with autoimmune diseases or after renal transplantation&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara">GS phenotype is characterized by hypokalemic alkalosis&#44; hypomagnesemia&#44; hypocalciuria&#44; and secondary aldosteronism without hypertension&#46; Hyponatraemia is not a recognised feature of GS&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">A 34 year old caucasian woman with no prior medical presented with severe hypokalemia&#59; hypomagnesemia and mild hyponatremia&#46; Her past medical and family history were unremarkable&#46; She was on no medication and denied any symptoms&#44; unless for occasionally muscle cramps&#46; Water intake &#8805;3L&#47;day&#46; She was normotensive&#44; no edemas and normal urine output&#46; The review of systems was otherwise negative&#46;</p><p class="elsevierStylePara">Table 1 summarizes laboratory investigation&#46;</p><p class="elsevierStylePara">Patient was managed with oral magnesium and spironolactone 50mg&#47;day&#46; Her condition improved significantly and her last routine lab control showed serum potassium 3&#46;78mmol&#47;L&#44; magnesium 0&#46;79mmol&#47;L and sodium 136&#46;0mmol&#47;L&#44; without any other changes&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Potassium excretion is mostly derived from secretion in the distal nephron&#44; driven by an electrochemical gradient increased by aldosterone-induced sodium reabsorption&#59; and by an electroneutral K<span class="elsevierStyleSup">&#43; </span>Cl<span class="elsevierStyleSup">- </span>secretory mechanism&#46;<span class="elsevierStyleSup">4</span></p><p class="elsevierStylePara">Hypokalemia may result from decreased intake&#44; increased translocation into the cells&#44; or&#44; most often&#44; increased losses in the urine&#44; gastrointestinal tract&#44; or sweat&#46;</p><p class="elsevierStylePara">Although these causes were sought by history taking and clinical examination&#44; we needed to exclude surreptitious vomiting or drugs abuse because high urinary potassium&#44; metabolic alkalosis and alkaline urine can also be present in these two disorders&#46; Differential diagnosis with vomiting was made through urinary chloride which is low in hypovolemia due to hyperaldosteronism&#44; opposing to patient normal values poiting to a renal disorder&#46; Diuretic abuse was excluded through a negative urinary screen&#46;</p><p class="elsevierStylePara">Because the patient was normotensive&#44; we stood with Gitelman or Bartter&#8217;s&#46;</p><p class="elsevierStylePara">Magnesium excretion rate is regulated by distal reabsorption that depends on epithelial TRPM6 channels&#44; which gene suffers a downregulation mutation in GS&#44; inducing urinary magnesium wasting leading to hypomagnesemia&#44;<span class="elsevierStyleSup">5</span> opposing to Bartter syndrome&#46;</p><p class="elsevierStylePara">Calcium is absorbed in proximal nephron driven by an electronegative transcellular gradient induced by chloride-sodium transport&#59; and in DCT driven by parathyroid hormone and Vitamin D&#46; Hypocalciuria pathogenesis still remains debated but an important role is played by metabolic alkalosis&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">At the end&#44; our patient fulfilled the diagnostic criteria for GS&#44; although few unusual aspects&#46; First&#44; the inappropriately high urine pH and pCO2 &#40;directly proportional to bicarbonate &#40;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">-</span>&#41; concentration&#41; could be explain through high chloride delivery that enhances HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">-</span> secretion in type A intercalated cells &#40;to maintain electroneutrality&#41;&#46; Adding to this&#44; hypokalemia suppresses aldosterone secretion&#44; which reduces sodium reabsorption &#40;no hypovolemia&#41; increasing back-diffusion of hydrogen&#44; allowing the urine to become more alkaline than plasma&#46;<span class="elsevierStyleSup">6</span> Aldosterone activity degree could be accessed through tubular fluid potassium concentration at distal cortical collecting tubule&#44; estimated from transtubular potassium gradient but this would only be usefull in hyperkalemia settings&#46; Additionaly&#44; recente publications found that its assumptions were not valid&#46;<span class="elsevierStyleSup">7</span> Finally&#44; patients with metabolic alkalosis have a respiratory compensation but the beneficial pH effect is blunted when arterial pCO<span class="elsevierStyleInf">2 </span>elevation increases renal acid excretion stimulating renal ammoniagenesis&#44; raising urine pH&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">Mild hyponatraemia was present and&#44; opposing to diuretic use &#40;excluded&#41;&#44; is not a typical feature of GS&#46; After excluding hypothyroidism&#44; adrenal insufficiency and renal failure&#44; hyponatraemia associated to normal volemia&#44; inappropriately high urine osmolality and urinary sodium concentration suggested the presence of a syndrome of inappropriate secretion of antidiuretic hormone &#40;SIADH&#41;&#46; The stimulus for this secretion is unclear&#46; Although chronic hypokalemia could be characterized by some resistance of tube collector cells to ADH&#44; GS has a urinary diluting capacity disturbed creating a <span class="elsevierStyleItalic">SIADH like effect</span>&#46; Opposing to Bartters&#44; GS has a preserved concentrating ability&#44;<span class="elsevierStyleSup">6</span> because medullary thick ascending limb is intact&#46; Since there is no hypovolemia&#44; urinary sodium excretion is high to maintain electroneutrality as HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">-</span> is being excreted&#46; Adding to this&#44; in severe hypokalemia&#44; via unknown mechanism&#44; distal chloride excretion is increased causing a paralell sodium waste&#46;</p><p class="elsevierStylePara">There are only a few cases of GS with hyponatraemia reported and in two of them a combination of high water intake with an impaired urinary dilution capacity caused by GS was described as a possible explanation for <span class="elsevierStyleItalic">SIADH-like</span> biochemical features&#46;<span class="elsevierStyleSup">8&#44;9</span> Adding to water&#44; our patient must had a high intake of salt which raised the sodium delivery to the collecting duct and could explain both sodium and HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">-</span> excretion increase&#44; with water free of electrolytes retention&#46; To the best of our knowledge it was what happened to our patient&#46;</p><p class="elsevierStylePara">A genetical study would confirm the diagnosis and clarify about additional anomalies but we didn&#8217;t performe it because of economic issues&#46; However&#44; we still don&#8217;t have many doubts about the diagnosis because there is a large phenotype variability without relationship between the clinical severity and type of mutations&#46; Furthermore&#44; heterozygotes have a higher rate of sodium excretion than wild-type individuals&#44; probably due to higher salt intake&#46;<span class="elsevierStyleSup">10</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12224&#95;16025&#95;52538&#95;en&#95;t1&#95;12224&#46;jpg" class="elsevierStyleCrossRefs"><img src="12224_16025_52538_en_t1_12224.jpg" alt="Results of the laboratory investigation&#46;"></img></a></p><p class="elsevierStylePara">Table 1&#46; Results of the laboratory investigation&#46;</p>"
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