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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Gitelman syndrome &#40;GS&#41; is a rare&#44; salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The disease is caused by inactivating mutations in the <span class="elsevierStyleItalic">SLC12A3</span> gene that encodes the thiazide-sensitive sodium-chloride cotransporter &#40;NCC&#41;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;3</span></a> and is recessively inherited&#46; The prevalence of GS is estimated to range around 25 cases per 1 million&#44; making it one of the most frequent inherited renal tubular disorders&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 35-year-old male&#44; with a history of seborrheic dermatitis treated with topical steroids and iron deficiency anemia was admitted with a first episode of biliary colic and hypokalemia &#40;2&#46;9 mEq&#47;L&#41;&#46; His electrolyte imbalance&#44; once the vomiting settled&#44; was challenging to manage with oral potassium supplements&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">He complained of thirst&#44; muscle weakness and fatigue with limited exertion&#46; He had occasional and doubtful arthritis&#46; At the time of the visit&#44; the patient did not present any gastrointestinal symptoms&#44; except reflux due to treatment with potassium&#44; but that was well controlled with a gastric protector&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The exploration was normal but on his electrocardiogram &#40;ECG&#41; we found a prominent U wave&#46; Blood tests showed normal renal function with serum creatinine 0&#46;81<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; glomerular filtration rate &#40;GFR&#41; 116<span class="elsevierStyleHsp" style=""></span>mL&#47;min per 1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#44; potassium 2&#46;9<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#44; sodium 141<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#44; chloride 98<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#44; phosphate 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; magnesium 1&#46;57<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; calcium 9&#46;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; mild elevation of white blood cell &#40;WBC&#41; count of 10&#44;640 per mm<span class="elsevierStyleSup">3</span> &#40;normal range 3500&#8211;10&#44;500 per mm<span class="elsevierStyleSup">3</span>&#41;&#44; hemoglobin 15&#46;2<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#44; liver function was normal&#44; plasma renin activity 1&#46;56<span class="elsevierStyleHsp" style=""></span>ng&#47;mL&#47;h with normosodic diet and supine position &#40;normal range 0&#46;2&#8211;2&#46;8<span class="elsevierStyleHsp" style=""></span>ng&#47;mL&#47;h&#41;&#44; metabolic alkalosis with pH 7&#46;50 and bicarbonate 30&#46;4<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#44; urinary sediment with mild density of 1008<span class="elsevierStyleHsp" style=""></span>g&#47;L and pH 8&#44; excretion in 24-h urine collection &#40;4200 mm<span class="elsevierStyleSup">3</span>&#41; 48<span class="elsevierStyleHsp" style=""></span>h without supplementation and diet of salt 5 grams showed glucose 105<span class="elsevierStyleHsp" style=""></span>mg&#44; uric acid 1210<span class="elsevierStyleHsp" style=""></span>mg&#44; creatinine 1617<span class="elsevierStyleHsp" style=""></span>mg&#44; potassium 232<span class="elsevierStyleHsp" style=""></span>mEq&#44; sodium 512<span class="elsevierStyleHsp" style=""></span>mEq&#44; chloride 326<span class="elsevierStyleHsp" style=""></span>mEq&#44; phosphate 1427<span class="elsevierStyleHsp" style=""></span>mg&#44; magnesium 227<span class="elsevierStyleHsp" style=""></span>mg&#44; calcium 81<span class="elsevierStyleHsp" style=""></span>mg&#44; protein excretion 0&#46;15<span class="elsevierStyleHsp" style=""></span>g confirmed and normal aminoaciduria&#46; Abdominal ultrasound showed kidneys with normal corticomedullary differentiation&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">A Next Generation Sequencing &#40;NGS&#41; Ion AmpliSeq&#8482; Custom Research Panel was used to study the coding regions and intronic flanking regions of the tubulopathy genes&#58; <span class="elsevierStyleItalic">CLCNKB</span>&#44; <span class="elsevierStyleItalic">CLCNKA</span>&#44; <span class="elsevierStyleItalic">SCL12A3</span>&#44; <span class="elsevierStyleItalic">SLC12A1</span>&#44; <span class="elsevierStyleItalic">KCNJ1</span>&#44; <span class="elsevierStyleItalic">BSND</span>&#44; <span class="elsevierStyleItalic">CASR</span>&#44; <span class="elsevierStyleItalic">CLDN16</span> and <span class="elsevierStyleItalic">CLDN19</span>&#46; Libraries were prepared using Ion Ampliseq Library kit 2&#46;0 &#40;Life Technologies&#44; CA&#44; USA&#41;&#46; Finally&#44; DNA high-throughput sequencing was performed on a Personal Genome Machine &#40;PGM&#41; using the Ion PGM&#8482; Hi-Q&#8482; Sequencing Kit &#40;Life Technologies&#41; on the Ion 318&#8482; sequencing chip &#40;Life Technologies&#41;&#46; Results evidenced a homozygous mutation c&#46;361G&#62;T &#40;p&#46;E121Ter&#59; <a id="intr0005" class="elsevierStyleInterRef" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&db=nucleotide&doptcmdl=genbank&term=NM_000339">NM&#95;000339</a>&#41; in the <span class="elsevierStyleItalic">SLC12A3</span> gene&#46; This nucleotide change results in a premature stop codon&#44; or a nonsense codon&#44; in the transcribed mRNA&#44; resulting in a truncated&#44; incomplete&#44; and usually nonfunctional protein&#46; This variant has not been previously reported&#46; Sanger sequencing of the exon 2 fragment confirmed that this patient was homozygous for the mutation&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">In the <span class="elsevierStyleItalic">SLC12A3</span> gene&#44; more than 180 mutations have been reported in GS patients&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> Sequencing of the <span class="elsevierStyleItalic">SLC12A3</span> exons is required to search for mutations in most GS patients because there is not a prevalent mutation&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">6&#44;7</span></a> Moreover&#44; CLCNKB mutations may be found in some cases with clinical manifestations of GS&#44; a fact that increases the complexity of the genetic study of GS&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">GS is inherited as an autosomal recessive trait&#44; and homozygous and combined heterozygous mutations are expected&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> In our case&#44; the single nucleotide polymorphism &#40;SNP&#41; detected along the <span class="elsevierStyleItalic">SLC12A3</span> gene was homozygous with the notion of consanguinity&#46; The p&#46;E121Ter variant was predicted to be likely pathogenic by at least three bioinformatic programs &#40;SIFT&#44; Polyphen and Mutation Taster&#41;&#46; The patient came from an isolated and small village in Spain&#44; and had a probable consanguinity between parents and a founder effect that has previously been reported in GS disease&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">The mutations impair the activity of thiazide-sensitive sodium-chloride cotransporter encoded by <span class="elsevierStyleItalic">SLC12A3</span> and could be classified in five different types according to their effect on the protein&#46; Large deletions including one or more exons of <span class="elsevierStyleItalic">SLC12A3</span> have also been detected<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> and the majority of these mutations should be included in this type 1 classification&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">The definition of the <span class="elsevierStyleItalic">SLC12A3</span> genotype through description of new mutations may be a useful tool in the clinical characterization of GS and in genetic counseling of salt-losing tubulopathies&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">First&#44; 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Letter to the Editor
Novel nonsense mutation in the SLC12A3 gene in a Spanish case of Gitelman syndrome
Nueva mutación finalizadora en el gen SLC12A3 en un caso de síndrome de Gitelman en España
Lourdes Roca-Argentea,
Corresponding author
lroca_argente@hotmail.com

Corresponding author.
, Angel Zúñigab, Jose Luis Moll-Guillema, Julio Hernández-Jarasa
a Department of Nephrology, La Fe University and Polytechnic Hospital, Valencia, Spain
b Department of Genetics, La Fe University and Polytechnic Hospital, Valencia, Spain
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        "titulo" => "Nueva mutaci&#243;n finalizadora en el gen SLC12A3 en un caso de s&#237;ndrome de Gitelman en Espa&#241;a"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Gitelman syndrome &#40;GS&#41; is a rare&#44; salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The disease is caused by inactivating mutations in the <span class="elsevierStyleItalic">SLC12A3</span> gene that encodes the thiazide-sensitive sodium-chloride cotransporter &#40;NCC&#41;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;3</span></a> and is recessively inherited&#46; The prevalence of GS is estimated to range around 25 cases per 1 million&#44; making it one of the most frequent inherited renal tubular disorders&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 35-year-old male&#44; with a history of seborrheic dermatitis treated with topical steroids and iron deficiency anemia was admitted with a first episode of biliary colic and hypokalemia &#40;2&#46;9 mEq&#47;L&#41;&#46; His electrolyte imbalance&#44; once the vomiting settled&#44; was challenging to manage with oral potassium supplements&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">He complained of thirst&#44; muscle weakness and fatigue with limited exertion&#46; He had occasional and doubtful arthritis&#46; At the time of the visit&#44; the patient did not present any gastrointestinal symptoms&#44; except reflux due to treatment with potassium&#44; but that was well controlled with a gastric protector&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The exploration was normal but on his electrocardiogram &#40;ECG&#41; we found a prominent U wave&#46; Blood tests showed normal renal function with serum creatinine 0&#46;81<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; glomerular filtration rate &#40;GFR&#41; 116<span class="elsevierStyleHsp" style=""></span>mL&#47;min per 1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#44; potassium 2&#46;9<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#44; sodium 141<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#44; chloride 98<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#44; phosphate 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; magnesium 1&#46;57<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; calcium 9&#46;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; mild elevation of white blood cell &#40;WBC&#41; count of 10&#44;640 per mm<span class="elsevierStyleSup">3</span> &#40;normal range 3500&#8211;10&#44;500 per mm<span class="elsevierStyleSup">3</span>&#41;&#44; hemoglobin 15&#46;2<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#44; liver function was normal&#44; plasma renin activity 1&#46;56<span class="elsevierStyleHsp" style=""></span>ng&#47;mL&#47;h with normosodic diet and supine position &#40;normal range 0&#46;2&#8211;2&#46;8<span class="elsevierStyleHsp" style=""></span>ng&#47;mL&#47;h&#41;&#44; metabolic alkalosis with pH 7&#46;50 and bicarbonate 30&#46;4<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#44; urinary sediment with mild density of 1008<span class="elsevierStyleHsp" style=""></span>g&#47;L and pH 8&#44; excretion in 24-h urine collection &#40;4200 mm<span class="elsevierStyleSup">3</span>&#41; 48<span class="elsevierStyleHsp" style=""></span>h without supplementation and diet of salt 5 grams showed glucose 105<span class="elsevierStyleHsp" style=""></span>mg&#44; uric acid 1210<span class="elsevierStyleHsp" style=""></span>mg&#44; creatinine 1617<span class="elsevierStyleHsp" style=""></span>mg&#44; potassium 232<span class="elsevierStyleHsp" style=""></span>mEq&#44; sodium 512<span class="elsevierStyleHsp" style=""></span>mEq&#44; chloride 326<span class="elsevierStyleHsp" style=""></span>mEq&#44; phosphate 1427<span class="elsevierStyleHsp" style=""></span>mg&#44; magnesium 227<span class="elsevierStyleHsp" style=""></span>mg&#44; calcium 81<span class="elsevierStyleHsp" style=""></span>mg&#44; protein excretion 0&#46;15<span class="elsevierStyleHsp" style=""></span>g confirmed and normal aminoaciduria&#46; Abdominal ultrasound showed kidneys with normal corticomedullary differentiation&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">A Next Generation Sequencing &#40;NGS&#41; Ion AmpliSeq&#8482; Custom Research Panel was used to study the coding regions and intronic flanking regions of the tubulopathy genes&#58; <span class="elsevierStyleItalic">CLCNKB</span>&#44; <span class="elsevierStyleItalic">CLCNKA</span>&#44; <span class="elsevierStyleItalic">SCL12A3</span>&#44; <span class="elsevierStyleItalic">SLC12A1</span>&#44; <span class="elsevierStyleItalic">KCNJ1</span>&#44; <span class="elsevierStyleItalic">BSND</span>&#44; <span class="elsevierStyleItalic">CASR</span>&#44; <span class="elsevierStyleItalic">CLDN16</span> and <span class="elsevierStyleItalic">CLDN19</span>&#46; Libraries were prepared using Ion Ampliseq Library kit 2&#46;0 &#40;Life Technologies&#44; CA&#44; USA&#41;&#46; Finally&#44; DNA high-throughput sequencing was performed on a Personal Genome Machine &#40;PGM&#41; using the Ion PGM&#8482; Hi-Q&#8482; Sequencing Kit &#40;Life Technologies&#41; on the Ion 318&#8482; sequencing chip &#40;Life Technologies&#41;&#46; Results evidenced a homozygous mutation c&#46;361G&#62;T &#40;p&#46;E121Ter&#59; <a id="intr0005" class="elsevierStyleInterRef" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&db=nucleotide&doptcmdl=genbank&term=NM_000339">NM&#95;000339</a>&#41; in the <span class="elsevierStyleItalic">SLC12A3</span> gene&#46; This nucleotide change results in a premature stop codon&#44; or a nonsense codon&#44; in the transcribed mRNA&#44; resulting in a truncated&#44; incomplete&#44; and usually nonfunctional protein&#46; This variant has not been previously reported&#46; Sanger sequencing of the exon 2 fragment confirmed that this patient was homozygous for the mutation&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">In the <span class="elsevierStyleItalic">SLC12A3</span> gene&#44; more than 180 mutations have been reported in GS patients&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> Sequencing of the <span class="elsevierStyleItalic">SLC12A3</span> exons is required to search for mutations in most GS patients because there is not a prevalent mutation&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">6&#44;7</span></a> Moreover&#44; CLCNKB mutations may be found in some cases with clinical manifestations of GS&#44; a fact that increases the complexity of the genetic study of GS&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">GS is inherited as an autosomal recessive trait&#44; and homozygous and combined heterozygous mutations are expected&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> In our case&#44; the single nucleotide polymorphism &#40;SNP&#41; detected along the <span class="elsevierStyleItalic">SLC12A3</span> gene was homozygous with the notion of consanguinity&#46; The p&#46;E121Ter variant was predicted to be likely pathogenic by at least three bioinformatic programs &#40;SIFT&#44; Polyphen and Mutation Taster&#41;&#46; The patient came from an isolated and small village in Spain&#44; and had a probable consanguinity between parents and a founder effect that has previously been reported in GS disease&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">The mutations impair the activity of thiazide-sensitive sodium-chloride cotransporter encoded by <span class="elsevierStyleItalic">SLC12A3</span> and could be classified in five different types according to their effect on the protein&#46; Large deletions including one or more exons of <span class="elsevierStyleItalic">SLC12A3</span> have also been detected<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> and the majority of these mutations should be included in this type 1 classification&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">The definition of the <span class="elsevierStyleItalic">SLC12A3</span> genotype through description of new mutations may be a useful tool in the clinical characterization of GS and in genetic counseling of salt-losing tubulopathies&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">First&#44; we suspected either GS or Bartter syndrome III the cause of hypokaliemia&#46; Other causes such as vomiting or the use of diuretics were rejected due to history&#46; The electrocardiographic alterations were probably secondary to hypokalemia&#46; The slight glucosuria present at the diagnosis reminds us that hypomagnesemia and hypokaliemia were speculated to cause impaired glucose tolerance in GS patients&#46; Our patient was not overweight&#44; had normal to low blood pressure&#44; and a proteinuria of 150<span class="elsevierStyleHsp" style=""></span>mg&#47;24<span class="elsevierStyleHsp" style=""></span>h was monitored because of the podocyte dysfunction link described&#46;</p></span>"
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Article information
ISSN: 20132514
Original language: English
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Nefrología (English Edition)
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?