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    "textoCompleto" => "<p class="elsevierStylePara">Dear Editor&#44;</p><p class="elsevierStylePara">Primary distal renal tubular acidosis &#40;dRTA&#41; is a tubule disease characterised by metabolic acidosis with inappropriately alkaline urine&#44; hypopotassaemia and hypercalciuria&#46; It may be sporadic or hereditary&#44; with a dominant or recessive autosomal pattern&#46; The severity of the clinical spectrum may vary greatly&#44; from slight&#44; asymptomatic compensated acidosis with an occasional calculus to severe acidosis with delayed growth and early onset nephrocalcinosis caused by kidney failure&#46; In general&#44; patients with dominant-pattern dRTA have a milder phenotype than those with a recessive pattern&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">A subgroup of recessive dRTA patients suffers from progressive neurosensory deafness&#44; caused by mutations in the gene that codifies sub-unit B1 in H&#43;-ATPase &#40;ATP6V1B1&#41;&#46;<span class="elsevierStyleSup">2 </span>The clinical profile for this tubular alteration&#44; besides the deafness&#44; is similar to that described for other types of dRTA&#46;</p><p class="elsevierStylePara">We present the clinical evolution of a patient with dRTA with neurosensory deafness and chronic kidney disease secondary to nephrocalcinosis over a 30-year follow-up period&#46;</p><p class="elsevierStylePara">Male patient aged 36&#46; A few days after birth his clinical profile included frequent vomiting&#44; polyuria&#44; polydypsia&#44; psychomotor delay&#44; hyperchloraemic metabolic acidosis&#44; hyperchloraemia&#44; hypopotassaemia&#44; alkaline urine and nephrocalcinosis&#44; and he was diagnosed with dRTA&#46; His family history included parents related by blood&#44; one sibling with dRTA who died in a workplace accident and another healthy sibling&#46;</p><p class="elsevierStylePara">The patient has been examined in our centre since he was six years old and receiving treatment with sodium citrate and oral potassium supplements&#46;</p><p class="elsevierStylePara">Laboratory analysis data of interest&#58; pH 7&#46;07-7&#46;33&#44; bicarbonate 10-26mmol&#47;L&#44; Cl 113-124mEq&#47;L&#44; K 1&#46;8-3&#46;5mEq&#47;L&#46; Magnesium&#44; calcium&#44; phosphorus&#44; ALP&#44; PTH and Vitamin D levels are normal&#46; Hb 12&#46;2-18&#46;7g&#47;dl&#44; Ht 38-55&#46;3&#37;&#46; Urine&#58; pH 7-8&#44; anion gap 43mEq&#47;l&#44; Calcium 2&#46;5-4&#46;5mg&#47;kg&#47;day&#44; Phosphorus 6-12mg&#47;kg&#47;day&#46; Urineplasma PCO2 difference&#58; 2mmHg &#40;urine pH&#58; 7&#46;25 and plasma pH&#58; 7&#46;33&#41;&#44; CaO&#47;CrO index&#58; 0&#46;16-0&#46;24&#46;</p><p class="elsevierStylePara">The patient&#191;s treatment was irregular&#59; he stopped taking his medication frequently&#44; and often did not attend check-ups&#46; This resulted in numerous admissions to hospital due to hypopotassaemic muscle paralysis and severe metabolic acidosis that would resolve quickly once bicarbonate and potassium treatment was administered&#46;</p><p class="elsevierStylePara">When the patient was 16&#44; a slow but progressive decrease in renal function began and the nephrocalcinosis became worse &#40;figure 1&#41;&#46; At 19&#44; hearing loss was detected&#59; the patient was diagnosed with bilateral neurosensory deafness&#44; and needed a hearing aid&#46;</p><p class="elsevierStylePara">At 25&#44; he developed bilateral renal lithiasis and complications and hospital admissions have been common over the last 10 years&#46; Most worthy of note are his bilateral renal colic episodes and the development of spontaneous steinstrasse&#44; which on some occasions resolved with spontaneous expulsion of the stones&#44; and on others required urethral catheterisation with a double J Stent and lithotripsy&#46; Several episodes caused obstruction of the urinary tract with hydronephrosis and acute renal failure added to his chronic kidney disease&#59; this resolved upon expulsion of the stones&#46;</p><p class="elsevierStylePara">The latest check-ups show a progressive increase of nephrocalcinosis&#46; There is also a parallel progressive increase of Hb and Ht levels currently with polycythaemia &#40;table 1&#41; and a normal EPO level &#40;11&#46;6mU&#47;ml&#41;&#46;</p><p class="elsevierStylePara">The patient currently maintains a stable creatinine clearance rate of about 45ml&#47;min&#46;</p><p class="elsevierStylePara">This case is important to us because our patient shows the main complications that can arise from this disease&#58; 1&#41; hypopotassaemic muscular paralysis as a result of discontinuing treatment frequently&#46; 2&#41; bilateral renal lithiasis&#44; which in turn has caused obstructive acute renal failure requiring multiple urinary tract procedures&#44; and has even provoked spontaneous steinstrasse&#44; which is seldom described in this type of patient&#46;<span class="elsevierStyleSup">3</span> 3&#41; polyglobulia&#44; probably secondary to nephrocalcinosis&#44; since the tissue hypoxia would induce an increase in EPO production which&#44; although still in the normal range in our case&#44; could be inappropriately high for such a high haemoglobin level&#46; In the literature&#44; this complication has very rarely been reported in association with dRTA&#59;<span class="elsevierStyleSup">4&#44;5</span> 4&#41; chronic kidney disease&#44; which in our case is progressing very slowly&#44; despite numerous complications &#40;20 years have passed since the creatinine clearing rate began to decrease&#41; and which has been stable over the last few years&#46;</p><p class="elsevierStylePara">We conclude that with dRTA&#44; supervising compliance with the treatment is very important for avoiding complications&#44; some of which are potentially severe and completely avoidable&#46; Paying attention to polycythaemia secondary to nephrocalcinosis is also crucial&#44; as the condition could foster the development of thrombotic events in these patients&#46; Despite everything&#44; the renal failure has been progressing very slowly over 30 years of observation&#46; </p><p class="elsevierStylePara"><a href="grande&#47;43318078&#95;t1&#95;pag499&#46;jpg" class="elsevierStyleCrossRefs"><img src="43318078_t1_pag499.jpg"></img></a></p><p class="elsevierStylePara">Table 1&#46; 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Distal renal tubular acidosis with neurosensory deafness. Clinical evolution after 30 years of follow-up
Acidosis tubular renal distal con sordera neurosensorial. Evolución clínica tras 30 años de seguimiento
Raquel López Hidalgoa, A.. Polo Moyanoa, M.. Manjón Rodrígueza, S.. Cerezo Moralesa
a Servicio de Nefrología, Hospital Universitario San Cecilio, Granada, Granada, España,
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    "textoCompleto" => "<p class="elsevierStylePara">Dear Editor&#44;</p><p class="elsevierStylePara">Primary distal renal tubular acidosis &#40;dRTA&#41; is a tubule disease characterised by metabolic acidosis with inappropriately alkaline urine&#44; hypopotassaemia and hypercalciuria&#46; It may be sporadic or hereditary&#44; with a dominant or recessive autosomal pattern&#46; The severity of the clinical spectrum may vary greatly&#44; from slight&#44; asymptomatic compensated acidosis with an occasional calculus to severe acidosis with delayed growth and early onset nephrocalcinosis caused by kidney failure&#46; In general&#44; patients with dominant-pattern dRTA have a milder phenotype than those with a recessive pattern&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">A subgroup of recessive dRTA patients suffers from progressive neurosensory deafness&#44; caused by mutations in the gene that codifies sub-unit B1 in H&#43;-ATPase &#40;ATP6V1B1&#41;&#46;<span class="elsevierStyleSup">2 </span>The clinical profile for this tubular alteration&#44; besides the deafness&#44; is similar to that described for other types of dRTA&#46;</p><p class="elsevierStylePara">We present the clinical evolution of a patient with dRTA with neurosensory deafness and chronic kidney disease secondary to nephrocalcinosis over a 30-year follow-up period&#46;</p><p class="elsevierStylePara">Male patient aged 36&#46; A few days after birth his clinical profile included frequent vomiting&#44; polyuria&#44; polydypsia&#44; psychomotor delay&#44; hyperchloraemic metabolic acidosis&#44; hyperchloraemia&#44; hypopotassaemia&#44; alkaline urine and nephrocalcinosis&#44; and he was diagnosed with dRTA&#46; His family history included parents related by blood&#44; one sibling with dRTA who died in a workplace accident and another healthy sibling&#46;</p><p class="elsevierStylePara">The patient has been examined in our centre since he was six years old and receiving treatment with sodium citrate and oral potassium supplements&#46;</p><p class="elsevierStylePara">Laboratory analysis data of interest&#58; pH 7&#46;07-7&#46;33&#44; bicarbonate 10-26mmol&#47;L&#44; Cl 113-124mEq&#47;L&#44; K 1&#46;8-3&#46;5mEq&#47;L&#46; Magnesium&#44; calcium&#44; phosphorus&#44; ALP&#44; PTH and Vitamin D levels are normal&#46; Hb 12&#46;2-18&#46;7g&#47;dl&#44; Ht 38-55&#46;3&#37;&#46; Urine&#58; pH 7-8&#44; anion gap 43mEq&#47;l&#44; Calcium 2&#46;5-4&#46;5mg&#47;kg&#47;day&#44; Phosphorus 6-12mg&#47;kg&#47;day&#46; Urineplasma PCO2 difference&#58; 2mmHg &#40;urine pH&#58; 7&#46;25 and plasma pH&#58; 7&#46;33&#41;&#44; CaO&#47;CrO index&#58; 0&#46;16-0&#46;24&#46;</p><p class="elsevierStylePara">The patient&#191;s treatment was irregular&#59; he stopped taking his medication frequently&#44; and often did not attend check-ups&#46; This resulted in numerous admissions to hospital due to hypopotassaemic muscle paralysis and severe metabolic acidosis that would resolve quickly once bicarbonate and potassium treatment was administered&#46;</p><p class="elsevierStylePara">When the patient was 16&#44; a slow but progressive decrease in renal function began and the nephrocalcinosis became worse &#40;figure 1&#41;&#46; At 19&#44; hearing loss was detected&#59; the patient was diagnosed with bilateral neurosensory deafness&#44; and needed a hearing aid&#46;</p><p class="elsevierStylePara">At 25&#44; he developed bilateral renal lithiasis and complications and hospital admissions have been common over the last 10 years&#46; Most worthy of note are his bilateral renal colic episodes and the development of spontaneous steinstrasse&#44; which on some occasions resolved with spontaneous expulsion of the stones&#44; and on others required urethral catheterisation with a double J Stent and lithotripsy&#46; Several episodes caused obstruction of the urinary tract with hydronephrosis and acute renal failure added to his chronic kidney disease&#59; this resolved upon expulsion of the stones&#46;</p><p class="elsevierStylePara">The latest check-ups show a progressive increase of nephrocalcinosis&#46; There is also a parallel progressive increase of Hb and Ht levels currently with polycythaemia &#40;table 1&#41; and a normal EPO level &#40;11&#46;6mU&#47;ml&#41;&#46;</p><p class="elsevierStylePara">The patient currently maintains a stable creatinine clearance rate of about 45ml&#47;min&#46;</p><p class="elsevierStylePara">This case is important to us because our patient shows the main complications that can arise from this disease&#58; 1&#41; hypopotassaemic muscular paralysis as a result of discontinuing treatment frequently&#46; 2&#41; bilateral renal lithiasis&#44; which in turn has caused obstructive acute renal failure requiring multiple urinary tract procedures&#44; and has even provoked spontaneous steinstrasse&#44; which is seldom described in this type of patient&#46;<span class="elsevierStyleSup">3</span> 3&#41; polyglobulia&#44; probably secondary to nephrocalcinosis&#44; since the tissue hypoxia would induce an increase in EPO production which&#44; although still in the normal range in our case&#44; could be inappropriately high for such a high haemoglobin level&#46; In the literature&#44; this complication has very rarely been reported in association with dRTA&#59;<span class="elsevierStyleSup">4&#44;5</span> 4&#41; chronic kidney disease&#44; which in our case is progressing very slowly&#44; despite numerous complications &#40;20 years have passed since the creatinine clearing rate began to decrease&#41; and which has been stable over the last few years&#46;</p><p class="elsevierStylePara">We conclude that with dRTA&#44; supervising compliance with the treatment is very important for avoiding complications&#44; some of which are potentially severe and completely avoidable&#46; Paying attention to polycythaemia secondary to nephrocalcinosis is also crucial&#44; as the condition could foster the development of thrombotic events in these patients&#46; Despite everything&#44; the renal failure has been progressing very slowly over 30 years of observation&#46; </p><p class="elsevierStylePara"><a href="grande&#47;43318078&#95;t1&#95;pag499&#46;jpg" class="elsevierStyleCrossRefs"><img src="43318078_t1_pag499.jpg"></img></a></p><p class="elsevierStylePara">Table 1&#46; 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