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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#58; </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Distal renal tubular acidosis &#40;DRTA&#41; is an acid-base balance disorder defined by the inability of the kidneys to compensate for the production of acids from protein metabolism by eliminating them&#44; due to decreased glomerular filtration &#40;GF&#41;&#46;</p><p class="elsevierStylePara">We report the case of a 33-year-old male patient with a history of hypokalaemia without study two years previously&#44; who was admitted to the Emergency Department due to 10 days of progressive weakness in his limbs&#44; fatigue&#44; asthaenia and myalgia and he denied experiencing urinary symptoms&#46; He self-medicated with potassium salts with no improvement&#44; and as such he decided to seek medical assistance&#46; On examination&#44; he had blood pressure of 119&#47;66mmHg&#44; heart rate of 67 beats&#47;minute&#44; respiratory rate of 22 breaths&#47;min&#44; a temperature of 37&#176;C&#44; with 3&#47;5 weakness in 4 limbs and diminished tendon reflexes&#46; His laboratory tests on admission showed serum creatinine of 1&#46;36mg&#47;dl&#44; serum sodium of 137mEq&#47;l potassium of 3&#46;2mEq&#47;l&#44; chloride of 114mEq&#47;l&#44; calcium of 8&#46;8mg&#47;dl&#44; phosphorus of 3&#46;5mg&#47;dl&#44; magnesium of 2&#46;2mEq&#47;l&#44; bicarbonate of 19mEq&#47;l&#44; pCO<span class="elsevierStyleInf">2</span> of 30mmHg&#44; venous pH of 7&#46;36&#44; lactate of 0&#46;8mEq&#47;l&#44; serum albumin of 4&#46;1g&#47;dl&#44; urine with a pH of 6&#46;5 without glucosuria and urinary sediment with minimal erythrocyturia and leukocyturia&#44; without nitrites or bacteria apparent in the microscope and proteinuria of 550mg&#47;24 hours&#46; We obtained a urine culture&#59; normal complement levels&#44; negative viral profile for human immunodeficiency virus and hepatitis B and C&#46; A renal ultrasound was performed and there were hyperechogenic images suggestive of medullary calcification &#40;Figure 1&#41;&#44; calciuria of 4&#46;2mg&#47;kg&#47;day&#44; positive urinary anion gap &#40;sodium of 58mEq&#47;l&#44; potassium of 16mEq&#47;l&#44; chloride of 23mEq&#47;l&#41;&#44; fractional excretion of potassium of 12&#37;&#44; fractional excretion of bicarbonate of 7&#37;&#44; but a urinary pH that failed to decrease to &#60;5&#46;5 over a period of more than 8 hours and reduction of the urinary gap&#44; but without becoming negative &#40;sodium of 47mEq&#47;l&#44; potassium of 12mEq&#47;l&#44; chlorine of 43mEq&#47;l&#41; after oral administration of ammonium chloride&#44; and as such it was classified as distal renal tubular acidosis &#40;DRTA&#41; &#40;type 1&#41;&#46; The urine culture was negative and as such percutaneous renal biopsy was performed&#44; which reported chronic tubulointerstitial nephritis with interstitial and intratubular nephrocalcinosis &#40;Figure 2&#41;&#46; The patient was therefore treated with 1mg&#47;kg&#47;day of prednisone and 1mEq&#47;kg&#47;day of potassium citrate&#46; A week later&#44; given a reduction in leukocyturia&#44; immunological studies reported positive anti-nuclear antibodies&#44; with a titre of 1&#58;2560&#44; positive anti-SSA and anti-SSB&#46; We performed Schirmer&#8217;s test&#44; which was positive&#44; curiously without dry eye symptoms&#46; In the outpatient follow-up after 16 weeks on 5mg&#47;day of prednisone&#44; the patient had creatinine of 0&#46;88mg&#47;dl and a decreased potassium salt requirement&#44; maintaining normal levels of potassium&#44; urinary pH at around 5&#44; calciuria of 3&#46;9mg&#47;kg&#47;day&#44; negative urinary anion gap &#40;sodium of 21mEq&#47;l&#44; potassium of 8mEq&#47;l&#44; chlorine of 47mEq&#47;l&#41;&#44; with the absence of leukocyturia&#44; erythrocyturia and proteinuria&#46;</p><p class="elsevierStylePara">Renal manifestations classified as renal tubular acidosis usually occur with a variable proportion between 3&#46;6&#37; and 73&#46;1&#37; in the series of patients with Sj&#246;gren&#39;s syndrome &#40;SS&#41; studied&#46;<span class="elsevierStyleSup">1</span> Acute and&#47;or chronic tubulointerstitial nephritis is the most common histopathological form in 54&#37;-80&#37; of cases&#46;<span class="elsevierStyleSup">1-3</span></p><p class="elsevierStylePara">In DRTA&#44; or type 1&#44; hypercalciuria is usually multifactorial &#40;release of bone calcium&#44; suppression of the calcium-sensing receptor &#91;CaSR&#93;&#44; increased distal sodium load and acidosis&#41;&#44; which along with alkaline urine and hypocitraturia favours calculi and nephrocalcinosis&#46; Initially normal GF may decrease over time due to dehydration&#44; nephrocalcinosis&#44; obstructive calculi and&#47;or infection&#46;<span class="elsevierStyleSup">4&#44;5</span></p><p class="elsevierStylePara">The objective of its treatment should be to normalise calciuria and citraturia to prevent nephrocalcinosis and progressive renal damage&#46; As such&#44; the underlying acidosis must be corrected&#46;<span class="elsevierStyleSup">5</span> Nevertheless&#44; this treatment is a palliative measure when its cause is secondary&#44; such as in SS&#44; where corticosteroids and cyclophosphamide have been used in accordance with the severity of renal involvement&#44; with reports of stabilised renal function&#44; a reduction in proteinuria and reversibility of various clinical manifestations deriving from renal tubular acidosis&#44; therefore preventing the extension of nephrocalcinosis and reducing the risk of progression to end-stage chronic kidney disease&#46;<span class="elsevierStyleSup">1&#44;2</span>&#46; In our case&#44; we used prednisone&#44; which was gradually reduced&#44; with a remission of clinical manifestations being achieved when the autoimmune tubulointerstitial nephritis deriving from SS was controlled&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span>&#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;12179&#95;16025&#95;52986&#95;en&#95;f112179&#46;jpg" class="elsevierStyleCrossRefs"><img src="12179_16025_52986_en_f112179.jpg" alt="Renal ultrasound with medullary hyperechogenicity suggestive of calcifications&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Renal ultrasound with medullary hyperechogenicity suggestive of calcifications&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12179&#95;16025&#95;52989&#95;en&#95;f2121792&#46;jpg" class="elsevierStyleCrossRefs"><img src="12179_16025_52989_en_f2121792.jpg" alt="Renal histopathology showing tubulointerstitial lymphoplasmacytic infiltrate &#40;A&#41; and intratubular and interstitial nephrocalcinosis with Von Kossa stain &#40;B&#41;&#46; Images at 40X&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Renal histopathology showing tubulointerstitial lymphoplasmacytic infiltrate &#40;A&#41; and intratubular and interstitial nephrocalcinosis with Von Kossa stain &#40;B&#41;&#46; Images at 40X&#46;</p>"
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Nephrocalcinosis and distal renal tubular acidosis in Sjögren's syndrome
Nefrocalcinosis y acidosis tubular renal distal en síndrome de Sjögren
Nasser A. Polancoa, M. Virgilia Soto-Abrahamb, Francisco E. Rodríguez-Castellanosc
a Servicio de Nefrología, Instituto Nacional de Cardiología Ignacio Chávez Ciudad de México, México,
b Servicio de Patología, Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México, México,
c Servicio de Nefrología, Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México, México,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#58; </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Distal renal tubular acidosis &#40;DRTA&#41; is an acid-base balance disorder defined by the inability of the kidneys to compensate for the production of acids from protein metabolism by eliminating them&#44; due to decreased glomerular filtration &#40;GF&#41;&#46;</p><p class="elsevierStylePara">We report the case of a 33-year-old male patient with a history of hypokalaemia without study two years previously&#44; who was admitted to the Emergency Department due to 10 days of progressive weakness in his limbs&#44; fatigue&#44; asthaenia and myalgia and he denied experiencing urinary symptoms&#46; He self-medicated with potassium salts with no improvement&#44; and as such he decided to seek medical assistance&#46; On examination&#44; he had blood pressure of 119&#47;66mmHg&#44; heart rate of 67 beats&#47;minute&#44; respiratory rate of 22 breaths&#47;min&#44; a temperature of 37&#176;C&#44; with 3&#47;5 weakness in 4 limbs and diminished tendon reflexes&#46; His laboratory tests on admission showed serum creatinine of 1&#46;36mg&#47;dl&#44; serum sodium of 137mEq&#47;l potassium of 3&#46;2mEq&#47;l&#44; chloride of 114mEq&#47;l&#44; calcium of 8&#46;8mg&#47;dl&#44; phosphorus of 3&#46;5mg&#47;dl&#44; magnesium of 2&#46;2mEq&#47;l&#44; bicarbonate of 19mEq&#47;l&#44; pCO<span class="elsevierStyleInf">2</span> of 30mmHg&#44; venous pH of 7&#46;36&#44; lactate of 0&#46;8mEq&#47;l&#44; serum albumin of 4&#46;1g&#47;dl&#44; urine with a pH of 6&#46;5 without glucosuria and urinary sediment with minimal erythrocyturia and leukocyturia&#44; without nitrites or bacteria apparent in the microscope and proteinuria of 550mg&#47;24 hours&#46; We obtained a urine culture&#59; normal complement levels&#44; negative viral profile for human immunodeficiency virus and hepatitis B and C&#46; A renal ultrasound was performed and there were hyperechogenic images suggestive of medullary calcification &#40;Figure 1&#41;&#44; calciuria of 4&#46;2mg&#47;kg&#47;day&#44; positive urinary anion gap &#40;sodium of 58mEq&#47;l&#44; potassium of 16mEq&#47;l&#44; chloride of 23mEq&#47;l&#41;&#44; fractional excretion of potassium of 12&#37;&#44; fractional excretion of bicarbonate of 7&#37;&#44; but a urinary pH that failed to decrease to &#60;5&#46;5 over a period of more than 8 hours and reduction of the urinary gap&#44; but without becoming negative &#40;sodium of 47mEq&#47;l&#44; potassium of 12mEq&#47;l&#44; chlorine of 43mEq&#47;l&#41; after oral administration of ammonium chloride&#44; and as such it was classified as distal renal tubular acidosis &#40;DRTA&#41; &#40;type 1&#41;&#46; The urine culture was negative and as such percutaneous renal biopsy was performed&#44; which reported chronic tubulointerstitial nephritis with interstitial and intratubular nephrocalcinosis &#40;Figure 2&#41;&#46; The patient was therefore treated with 1mg&#47;kg&#47;day of prednisone and 1mEq&#47;kg&#47;day of potassium citrate&#46; A week later&#44; given a reduction in leukocyturia&#44; immunological studies reported positive anti-nuclear antibodies&#44; with a titre of 1&#58;2560&#44; positive anti-SSA and anti-SSB&#46; We performed Schirmer&#8217;s test&#44; which was positive&#44; curiously without dry eye symptoms&#46; In the outpatient follow-up after 16 weeks on 5mg&#47;day of prednisone&#44; the patient had creatinine of 0&#46;88mg&#47;dl and a decreased potassium salt requirement&#44; maintaining normal levels of potassium&#44; urinary pH at around 5&#44; calciuria of 3&#46;9mg&#47;kg&#47;day&#44; negative urinary anion gap &#40;sodium of 21mEq&#47;l&#44; potassium of 8mEq&#47;l&#44; chlorine of 47mEq&#47;l&#41;&#44; with the absence of leukocyturia&#44; erythrocyturia and proteinuria&#46;</p><p class="elsevierStylePara">Renal manifestations classified as renal tubular acidosis usually occur with a variable proportion between 3&#46;6&#37; and 73&#46;1&#37; in the series of patients with Sj&#246;gren&#39;s syndrome &#40;SS&#41; studied&#46;<span class="elsevierStyleSup">1</span> Acute and&#47;or chronic tubulointerstitial nephritis is the most common histopathological form in 54&#37;-80&#37; of cases&#46;<span class="elsevierStyleSup">1-3</span></p><p class="elsevierStylePara">In DRTA&#44; or type 1&#44; hypercalciuria is usually multifactorial &#40;release of bone calcium&#44; suppression of the calcium-sensing receptor &#91;CaSR&#93;&#44; increased distal sodium load and acidosis&#41;&#44; which along with alkaline urine and hypocitraturia favours calculi and nephrocalcinosis&#46; Initially normal GF may decrease over time due to dehydration&#44; nephrocalcinosis&#44; obstructive calculi and&#47;or infection&#46;<span class="elsevierStyleSup">4&#44;5</span></p><p class="elsevierStylePara">The objective of its treatment should be to normalise calciuria and citraturia to prevent nephrocalcinosis and progressive renal damage&#46; As such&#44; the underlying acidosis must be corrected&#46;<span class="elsevierStyleSup">5</span> Nevertheless&#44; this treatment is a palliative measure when its cause is secondary&#44; such as in SS&#44; where corticosteroids and cyclophosphamide have been used in accordance with the severity of renal involvement&#44; with reports of stabilised renal function&#44; a reduction in proteinuria and reversibility of various clinical manifestations deriving from renal tubular acidosis&#44; therefore preventing the extension of nephrocalcinosis and reducing the risk of progression to end-stage chronic kidney disease&#46;<span class="elsevierStyleSup">1&#44;2</span>&#46; In our case&#44; we used prednisone&#44; which was gradually reduced&#44; with a remission of clinical manifestations being achieved when the autoimmune tubulointerstitial nephritis deriving from SS was controlled&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span>&#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;12179&#95;16025&#95;52986&#95;en&#95;f112179&#46;jpg" class="elsevierStyleCrossRefs"><img src="12179_16025_52986_en_f112179.jpg" alt="Renal ultrasound with medullary hyperechogenicity suggestive of calcifications&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Renal ultrasound with medullary hyperechogenicity suggestive of calcifications&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12179&#95;16025&#95;52989&#95;en&#95;f2121792&#46;jpg" class="elsevierStyleCrossRefs"><img src="12179_16025_52989_en_f2121792.jpg" alt="Renal histopathology showing tubulointerstitial lymphoplasmacytic infiltrate &#40;A&#41; and intratubular and interstitial nephrocalcinosis with Von Kossa stain &#40;B&#41;&#46; Images at 40X&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Renal histopathology showing tubulointerstitial lymphoplasmacytic infiltrate &#40;A&#41; and intratubular and interstitial nephrocalcinosis with Von Kossa stain &#40;B&#41;&#46; Images at 40X&#46;</p>"
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