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        "titulo" => "Informe de casos de acidosis tubular renal y errores de diagn&#243;stico"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Renal tubular acidosis &#40;RTA&#41; is a pathophysiological alteration of acid&#8211;base metabolism&#44; characterised by the presence of hyperchloraemic metabolic acidosis&#44; which is caused by renal loss of bicarbonate or a reduction in hydrogen ion excretion by the renal tubules&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> A suspicion of RTA is based on the clinical presentation of various signs and symptoms such as anorexia&#44; vomiting&#44; polyuria&#44; polydipsia&#44; delayed growth&#44; muscle weakness&#44; rickets&#44; nephrocalcinosis and sensorineural deafness&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> The diagnosis is validated with laboratory examinations that should include the demonstration of hyperchloraemic metabolic acidosis&#44; with a normal blood anion gap and a blood pH lower than 7&#46;35&#44; in patients with decompensated metabolic acidosis&#46; In the case of secondary RTA&#44; it is important to diagnose the systemic disease that is causing it&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> It should be noted that intestinal losses of bicarbonate&#44; whether they are due to diarrhoea or a fistula&#44; are a common cause of the same acid&#8211;base alterations&#44; and so they should not be present when a diagnosis of RTA is made&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">RTA has been reported to be overdiagnosed in Mexico&#44;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> and it has been associated with allergy&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#8211;6</span></a> For this reason&#44; we conducted a study with the aim of documenting the diagnosis of RTA in children from different hospitals&#46; A total of 170 children with a prior diagnosis of RTA were enrolled&#59; the majority were receiving alkaline treatment&#46; Treatment was suspended 5 to 7 days prior to the initial assessment&#44; which consisted of a medical history&#44; laboratory examinations and an assessment by the allergy department&#46; A diagnosis of RTA was only confirmed in 3 patients &#40;1&#46;8&#37;&#41;&#44; one with distal RTA and 2 with RTA secondary to cystinosis&#44; which were accompanied by Fanconi syndrome&#46; None of them had an allergy&#46; The rest of the patients&#8217; prior diagnosis of RTA was erroneous&#59; failure to thrive was caused by other conditions such as nutritional deficiency&#44; Turner syndrome&#44; giardiasis&#44; coeliac disease&#44; familial short stature&#44; hypophosphataemic rickets&#44; coenzyme Q10 deficiency or cardiomyopathy&#46; The cases with RTA are described below&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Case 1&#58;</span> A 12-year-old eutrophic female patient with normal anthropometric measurements for her age and gender&#46; She was diagnosed with RTA at one month of age&#44; and since then she has been receiving a potassium citrate solution&#46; On the third day of suspending alkaline treatment she had vomiting&#44; metabolic acidosis&#44; blood pH 7&#46;22&#59; &#91;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">&#8722;</span>&#93; 10<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#59; blood anion gap 11&#59; K<span class="elsevierStyleSup">&#43;</span> 2&#46;2<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; Cl<span class="elsevierStyleSup">&#8722;</span> 114<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; urine calcium&#47;creatinine 1&#46;38&#59; urinary pH&#58; 7&#46;5&#46; Alkaline treatment &#8212; bicarbonate and potassium &#8212; was restarted&#46; Kidney ultrasound&#58; grade III medullary nephrocalcinosis&#46; Molecular study&#58; mutation of the <span class="elsevierStyleItalic">ATPV60A4</span> gene&#44; not previously reported in the literature&#44; which shall be the subject of a subsequent publication&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Case 2&#58;</span> A 22-month-old male patient with delayed growth since sixth months of age&#46; At 11 months&#44; he was diagnosed with distal ATR&#44; with vomiting&#44; polydipsia and polyuria&#44; and he received treatment with a potassium citrate solution&#46; Entry into the study&#58; weight 7&#46;88<span class="elsevierStyleHsp" style=""></span>kg &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; height 71<span class="elsevierStyleHsp" style=""></span>cm &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; weight&#47;age 71&#37;&#59; weight&#47;height 86&#46;3&#37;&#59; height&#47;age 91&#46;8&#37;&#59; BMI <span class="elsevierStyleItalic">Z</span>-score&#58; &#8722;1&#46;47&#46; Blood gases pH 7&#46;39&#59; &#91;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">&#8722;</span>&#93; 16&#46;2<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#59; K<span class="elsevierStyleSup">&#43;</span> 3&#46;0<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#8722;</span> 2&#46;4<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; urine pH&#58; 7&#46;5&#59; trace albumin&#44; &#43;glucosuria&#59; microscopic haematuria&#44; 45&#37; tubular reabsorption of phosphate&#46; Administration of furosemide&#58; did not have urinary acidification&#46; Ophthalmology&#58; birefringent crystals in the cornea with a slit lamp&#46; A diagnosis of infantile nephropathic cystinosis was considered&#46; Molecular study of the <span class="elsevierStyleItalic">CTNS</span> gene &#40;17p13&#44; NG&#95;012489&#46;1 RefSeqGene&#41;&#58; compound heterozygous genotype&#44; predictor of severe form of infantile nephropathic cystinosis with deletion of 57<span class="elsevierStyleHsp" style=""></span>kb&#44; deletion of the first 10 exons&#44; mutation more common in Caucasian&#44; Mexican and Latin American patients<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7&#44;8</span></a> with cystinosis and a minor deletion previously reported in European populations&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Treatment with cysteamine bitartrate&#44; phosphates&#44; bicarbonate and potassium&#44; with satisfactory evolution&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Case 3&#58;</span> A 20-month-old female patient with polyuria&#44; polydipsia&#44; anorexia and delayed growth&#46; RTA was suspected&#44; and she was referred to our institution without being treated&#46; Weight 6&#46;9<span class="elsevierStyleHsp" style=""></span>kg &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; height 75&#46;5<span class="elsevierStyleHsp" style=""></span>cm &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; weight&#47;age 60&#46;9&#37;&#59; weight&#47;height 73&#37;&#59; height&#47;age 91&#46;3&#37;&#46; Blood gases&#58; pH 7&#46;47&#59; &#91;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">&#8722;</span>&#93; 13&#46;8<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#59; K<span class="elsevierStyleSup">&#43;</span> 3&#46;6<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#8722;</span> 2&#46;2<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; Cl<span class="elsevierStyleSup">&#8722;</span> 114<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; urine pH 7&#46;0&#59; glucosuria 100<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; &#43;albumin&#46; Ophthalmology&#58; birefringent corneal cystine crystals&#46; Molecular study of the <span class="elsevierStyleItalic">CTNS</span> gene&#58; homozygous genotype&#44; microdeletion of exon 12&#44; which deleted amino acids 346&#8211;349 of the 7th transmembrane domain of cystinosin&#44; which confirmed the diagnosis of infantile nephropathic cystinosis&#44; reported in Europeans<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a>&#46; Treatment with cysteamine bitartrate&#44; phosphates&#44; bicarbonate and potassium&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">We concluded that RTA is an uncommon tubulopathy&#44; not associated with allergy&#44; and confirmed that it is overdiagnosed in Mexico&#46; We recommend a comprehensive paediatric approach in children with delayed growth&#44; considering other diseases in addition to RTA&#44; with special caution in the studies that are requested and their quality&#46; When RTA is diagnosed&#44; the presence of primary diseases with secondary RTA should be ruled out&#44; and suitable guidance and nutritional support should be provided&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0035" class="elsevierStylePara elsevierViewall">The study was funded by <span class="elsevierStyleGrantSponsor" id="gs1">Federal Funds for Hospital Infantil de M&#233;xico Federico G&#243;mez</span> protocol HIM&#47;2012&#47;036&#46; Molecular study of the <span class="elsevierStyleItalic">CTNS</span> gene for patients with cystinosis was funded by <span class="elsevierStyleGrantSponsor" id="gs2">Federal Research Funds of the Mexican National Institute of Paediatrics</span> &#40;INP&#41; &#40;Modality A&#44; summons 2014&#8211;2015&#41;&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors have no conflict of interest to declare&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Medeiros M&#44; Enciso S&#44; Hern&#225;ndez AM&#44; Hern&#225;ndez HRG&#44; Toussaint G&#44; Pinto C&#44; et al&#46; Informe de casos de acidosis tubular renal y errores de diagn&#243;stico&#46; Nefrolog&#237;a&#46; 2016&#59;36&#58;323&#8211;325&#46;</p>"
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                            2 => "R&#46; Garcia-Caballero"
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Letter to the Editor – Brief Case Reports
Case reports and misdiagnosis of renal tubular acidosis
Informe de casos de acidosis tubular renal y errores de diagnóstico
Mara Medeirosa,b,
Corresponding author
, Sandra Encisoa, Ana María Hernándeza, Hector Rodrigo García Hernándeza, Georgina Toussainta, Claudia Pintoc, Elsy Maureen Navarrete Rodríguezd, Blanca E. del-Rio-Navarrod, Omar Josué Saucedo-Ramírezd, Patricia Medina Bravoe, Sergio Mirandaf, Liliana Woronaf, Germán Sosac, Leticia Belmont Martinezg, Miguel Ángel Alcántara Ortigozah, Laura Escobari, Ricardo Muñoz Arizpea
a Laboratorio de Investigación en Nefrología y Metabolismo Mineral Óseo, Hospital Infantil de México Federico Gómez, México, D.F., Mexico
b Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, México, D.F., Mexico
c Departamento de Nefrología «Dr. Gustavo Gordillo Paniagua», Hospital. Infantil de México Federico Gómez, México, D.F., Mexico
d Servicio de Alergia e Inmunología Clínica Pediátrica, Hospital Infantil de México Federico Gómez, México, D.F., Mexico
e Departamento de Endocrinología, Hospital Infantil de México Federico Gómez, México, D.F., Mexico
f Departamento de Gastroenterología, Hospital Infantil de México Federico Gómez, México, D.F., Mexico
g Laboratorio de Errores Innatos del Metabolismo y Tamiz, Instituto Nacional de Pediatría, México, D.F., Mexico
h Departamento de Biología Molecular, Instituto Nacional de Pediatría, México, D.F., Mexico
i Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México, D.F., Mexico
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        "titulo" => "Informe de casos de acidosis tubular renal y errores de diagn&#243;stico"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Renal tubular acidosis &#40;RTA&#41; is a pathophysiological alteration of acid&#8211;base metabolism&#44; characterised by the presence of hyperchloraemic metabolic acidosis&#44; which is caused by renal loss of bicarbonate or a reduction in hydrogen ion excretion by the renal tubules&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> A suspicion of RTA is based on the clinical presentation of various signs and symptoms such as anorexia&#44; vomiting&#44; polyuria&#44; polydipsia&#44; delayed growth&#44; muscle weakness&#44; rickets&#44; nephrocalcinosis and sensorineural deafness&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> The diagnosis is validated with laboratory examinations that should include the demonstration of hyperchloraemic metabolic acidosis&#44; with a normal blood anion gap and a blood pH lower than 7&#46;35&#44; in patients with decompensated metabolic acidosis&#46; In the case of secondary RTA&#44; it is important to diagnose the systemic disease that is causing it&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> It should be noted that intestinal losses of bicarbonate&#44; whether they are due to diarrhoea or a fistula&#44; are a common cause of the same acid&#8211;base alterations&#44; and so they should not be present when a diagnosis of RTA is made&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">RTA has been reported to be overdiagnosed in Mexico&#44;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> and it has been associated with allergy&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#8211;6</span></a> For this reason&#44; we conducted a study with the aim of documenting the diagnosis of RTA in children from different hospitals&#46; A total of 170 children with a prior diagnosis of RTA were enrolled&#59; the majority were receiving alkaline treatment&#46; Treatment was suspended 5 to 7 days prior to the initial assessment&#44; which consisted of a medical history&#44; laboratory examinations and an assessment by the allergy department&#46; A diagnosis of RTA was only confirmed in 3 patients &#40;1&#46;8&#37;&#41;&#44; one with distal RTA and 2 with RTA secondary to cystinosis&#44; which were accompanied by Fanconi syndrome&#46; None of them had an allergy&#46; The rest of the patients&#8217; prior diagnosis of RTA was erroneous&#59; failure to thrive was caused by other conditions such as nutritional deficiency&#44; Turner syndrome&#44; giardiasis&#44; coeliac disease&#44; familial short stature&#44; hypophosphataemic rickets&#44; coenzyme Q10 deficiency or cardiomyopathy&#46; The cases with RTA are described below&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Case 1&#58;</span> A 12-year-old eutrophic female patient with normal anthropometric measurements for her age and gender&#46; She was diagnosed with RTA at one month of age&#44; and since then she has been receiving a potassium citrate solution&#46; On the third day of suspending alkaline treatment she had vomiting&#44; metabolic acidosis&#44; blood pH 7&#46;22&#59; &#91;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">&#8722;</span>&#93; 10<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#59; blood anion gap 11&#59; K<span class="elsevierStyleSup">&#43;</span> 2&#46;2<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; Cl<span class="elsevierStyleSup">&#8722;</span> 114<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; urine calcium&#47;creatinine 1&#46;38&#59; urinary pH&#58; 7&#46;5&#46; Alkaline treatment &#8212; bicarbonate and potassium &#8212; was restarted&#46; Kidney ultrasound&#58; grade III medullary nephrocalcinosis&#46; Molecular study&#58; mutation of the <span class="elsevierStyleItalic">ATPV60A4</span> gene&#44; not previously reported in the literature&#44; which shall be the subject of a subsequent publication&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Case 2&#58;</span> A 22-month-old male patient with delayed growth since sixth months of age&#46; At 11 months&#44; he was diagnosed with distal ATR&#44; with vomiting&#44; polydipsia and polyuria&#44; and he received treatment with a potassium citrate solution&#46; Entry into the study&#58; weight 7&#46;88<span class="elsevierStyleHsp" style=""></span>kg &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; height 71<span class="elsevierStyleHsp" style=""></span>cm &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; weight&#47;age 71&#37;&#59; weight&#47;height 86&#46;3&#37;&#59; height&#47;age 91&#46;8&#37;&#59; BMI <span class="elsevierStyleItalic">Z</span>-score&#58; &#8722;1&#46;47&#46; Blood gases pH 7&#46;39&#59; &#91;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">&#8722;</span>&#93; 16&#46;2<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#59; K<span class="elsevierStyleSup">&#43;</span> 3&#46;0<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#8722;</span> 2&#46;4<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; urine pH&#58; 7&#46;5&#59; trace albumin&#44; &#43;glucosuria&#59; microscopic haematuria&#44; 45&#37; tubular reabsorption of phosphate&#46; Administration of furosemide&#58; did not have urinary acidification&#46; Ophthalmology&#58; birefringent crystals in the cornea with a slit lamp&#46; A diagnosis of infantile nephropathic cystinosis was considered&#46; Molecular study of the <span class="elsevierStyleItalic">CTNS</span> gene &#40;17p13&#44; NG&#95;012489&#46;1 RefSeqGene&#41;&#58; compound heterozygous genotype&#44; predictor of severe form of infantile nephropathic cystinosis with deletion of 57<span class="elsevierStyleHsp" style=""></span>kb&#44; deletion of the first 10 exons&#44; mutation more common in Caucasian&#44; Mexican and Latin American patients<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7&#44;8</span></a> with cystinosis and a minor deletion previously reported in European populations&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Treatment with cysteamine bitartrate&#44; phosphates&#44; bicarbonate and potassium&#44; with satisfactory evolution&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Case 3&#58;</span> A 20-month-old female patient with polyuria&#44; polydipsia&#44; anorexia and delayed growth&#46; RTA was suspected&#44; and she was referred to our institution without being treated&#46; Weight 6&#46;9<span class="elsevierStyleHsp" style=""></span>kg &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; height 75&#46;5<span class="elsevierStyleHsp" style=""></span>cm &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>3&#41;&#59; weight&#47;age 60&#46;9&#37;&#59; weight&#47;height 73&#37;&#59; height&#47;age 91&#46;3&#37;&#46; Blood gases&#58; pH 7&#46;47&#59; &#91;HCO<span class="elsevierStyleInf">3</span><span class="elsevierStyleSup">&#8722;</span>&#93; 13&#46;8<span class="elsevierStyleHsp" style=""></span>mmol&#47;l&#59; K<span class="elsevierStyleSup">&#43;</span> 3&#46;6<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; HPO<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#8722;</span> 2&#46;2<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; Cl<span class="elsevierStyleSup">&#8722;</span> 114<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#59; urine pH 7&#46;0&#59; glucosuria 100<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; &#43;albumin&#46; Ophthalmology&#58; birefringent corneal cystine crystals&#46; Molecular study of the <span class="elsevierStyleItalic">CTNS</span> gene&#58; homozygous genotype&#44; microdeletion of exon 12&#44; which deleted amino acids 346&#8211;349 of the 7th transmembrane domain of cystinosin&#44; which confirmed the diagnosis of infantile nephropathic cystinosis&#44; reported in Europeans<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a>&#46; Treatment with cysteamine bitartrate&#44; phosphates&#44; bicarbonate and potassium&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">We concluded that RTA is an uncommon tubulopathy&#44; not associated with allergy&#44; and confirmed that it is overdiagnosed in Mexico&#46; We recommend a comprehensive paediatric approach in children with delayed growth&#44; considering other diseases in addition to RTA&#44; with special caution in the studies that are requested and their quality&#46; When RTA is diagnosed&#44; the presence of primary diseases with secondary RTA should be ruled out&#44; and suitable guidance and nutritional support should be provided&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0035" class="elsevierStylePara elsevierViewall">The study was funded by <span class="elsevierStyleGrantSponsor" id="gs1">Federal Funds for Hospital Infantil de M&#233;xico Federico G&#243;mez</span> protocol HIM&#47;2012&#47;036&#46; Molecular study of the <span class="elsevierStyleItalic">CTNS</span> gene for patients with cystinosis was funded by <span class="elsevierStyleGrantSponsor" id="gs2">Federal Research Funds of the Mexican National Institute of Paediatrics</span> &#40;INP&#41; &#40;Modality A&#44; summons 2014&#8211;2015&#41;&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors have no conflict of interest to declare&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Medeiros M&#44; Enciso S&#44; Hern&#225;ndez AM&#44; Hern&#225;ndez HRG&#44; Toussaint G&#44; Pinto C&#44; et al&#46; Informe de casos de acidosis tubular renal y errores de diagn&#243;stico&#46; Nefrolog&#237;a&#46; 2016&#59;36&#58;323&#8211;325&#46;</p>"
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ISSN: 20132514
Original language: English
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