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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44; </span></p><p class="elsevierStylePara">The use of acetazolamide for the treatment of Meniere&#8217;s syndrome<span class="elsevierStyleSup">1&#44;2</span> is uncommon&#44; since other drugs constitute the first line used in the treatment of this pathology&#46;</p><p class="elsevierStylePara">Here we present the case of a 70-year old woman whose most relevant background involved Meniere&#8217;s syndrome&#44; currently treated with acetazolamide at 250mg&#47;12h with oral potassium supplements&#46;</p><p class="elsevierStylePara">The patient was referred to us due to severe renal failure &#40;urea&#58; 194mg&#47;dl&#59; C-reactive protein&#58; 8&#46;1mg&#47;dl&#41;&#44; with extremely severe metabolic acidosis &#40;venous gas&#58; pH&#58; 7&#46;1&#44; bicarbonate&#58; 6&#46;5mmol&#47;l&#44; PCO<span class="elsevierStyleInf">2</span>&#58; 18mm Hg&#44; PO<span class="elsevierStyleInf">2</span>&#58; 69mm Hg&#41; and anuria&#46; Laboratory analyses from a few months prior indicated C-reactive protein of 1mg&#47;dl&#46; The patient had been admitted to the nearest reference hospital 24 hours before as a result of severe diarrhoea&#44; and continued taking the normal treatment&#46; Hydration treatment had been started without diuresis&#44; and the patient was transferred for monitoring&#46; Upon hospitalisation&#44; dehydration signs were present&#44; with a blood pressure of 80&#47;50mm Hg&#44; anuria&#44; and no fever&#46; At this point the patient did not have diarrhoea&#46;</p><p class="elsevierStylePara">Laboratory analysis revealed acidosis&#44; hypokalaemia &#40;K&#58; 2&#46;9mEq&#47;l&#41; and renal failure similar to that described&#46; We continued to provide intense rehydration therapy&#44; despite which the patient continued with anuria for 24 hours more&#44; with C-reactive protein levels reaching 11mg&#47;dl&#46; Once the volume level was normalised&#44; diuresis started to improve&#44; with clinical and laboratory improvements until reaching a C-reactive protein of 1&#46;2mg&#47;dl upon discharge&#44; with a complete acid-base correction&#46; The evolution of the laboratory values are shown in Table 1&#46;</p><p class="elsevierStylePara">The patient was discharged with the diagnosis of prerenal acute renal failure due to severe hydrosaline depletion&#46; Metabolic acidosis with a normal anion-gap&#44; in the context of acute renal failure due to the ingestion of acetazolamide and diarrhoea&#46;</p><p class="elsevierStylePara">Metabolic acidosis is defined as a process in which the blood pH decreases&#44; with the first effect of decreased bicarbonate concentrations followed by the secondary effect of reduced PCO<span class="elsevierStyleInf">2</span>&#46; Our patient was admitted with acidosis&#58; a pH of 7&#46;1 and a bicarbonate level of 6mEq&#47;l&#46; The acidaemia caused increased ventilation that induced a hypocapnic response that tends to normalise pH&#46; The level of compensation expected can be deduced from the following formula&#58; pCO<span class="elsevierStyleInf">2 </span>&#61; 1&#46;5 &#91;HCO<span class="elsevierStyleInf">3</span>&#93; &#43; 8 &#40;&#177; 2&#41;&#46; In our patient&#44; the level of compensation was adequate &#40;pCO<span class="elsevierStyleInf">2</span>&#58; 17mm Hg&#41;&#44; and so this was a case of pure metabolic acidosis&#44; with correct respiratory compensation&#46;<span class="elsevierStyleSup">3&#44;4</span></p><p class="elsevierStylePara">The patient&#8217;s anion gap upon hospitalisation was normal&#44; near 12&#46; The cases of metabolic acidosis with a normal anion <span class="elsevierStyleItalic">gap</span> &#40;hyperchloremic&#41; suggest that bicarbonate has been replaced by chlorine as it is lost&#46; The most common causes of this type of acidosis are gastrointestinal loss through diarrhoea and renal loss which&#44; in our case&#44; were both caused by acetazolamide&#46;</p><p class="elsevierStylePara">The patient had low potassium levels&#44; lost through the faeces&#44; and volume depletion that increase the synthesis of renin and aldosterone&#44; which in turn raises the renal secretion rate of potassium&#44; in this case&#44; upon admission&#44; to 2&#46;9mEq&#47;l despite oral supplements&#46; Instead of acidic urine we can observe urine pH of six or higher because the metabolic acidosis and hypokalaemia increase the renal excretion and synthesis of NH<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#43; </span>and in turn buffers the H<span class="elsevierStyleSup">&#43; </span>and increases urine pH&#46; The fractional excretion of sodium tends to be low &#40;&#60;1&#37;-2&#37;&#41; in patients with gastrointestinal losses of HCO<span class="elsevierStyleInf">3</span>&#44; although this value was high in our patient&#44; without the classic inversion of sodium&#47;potassium in urine samples typical of prerenal conditions due to the combined effects of diarrhoea and diuretics&#46;<span class="elsevierStyleSup">5&#44;6</span></p><p class="elsevierStylePara">In the case that proximal reabsorption of bicarbonate is ineffective due to the use of acetazolamide&#44; which inhibits carbonic anhydrase&#44; bicarbonate losses are produced&#44; such that this molecule escapes from the proximal tubule and reaches the cortical collecting tubule or the distal convoluted tubule&#44; producing reabsorption of sodium and excretion of potassium and hydrogen ions&#46; The low permeability of bicarbonate impedes its reabsorption&#44; which creates a negative potential in the tubular lumen that increases the excretion of potassium and hydrogen ions&#46;</p><p class="elsevierStylePara">With regard to treatment&#44; the correct approach is to treat the diarrhoea&#44; as well as hydrosaline correction in order to halt the perpetuating stimulus of the renin-angiotensin-aldosterone pathway&#44; with the use of bicarbonate in a continuous perfusion and potassium chloride in order to replace the lost potassium&#44; along with the evident removal of the diuretics&#46; In this manner&#44; our patient responded satisfactorily&#44; with an excellent clinical evolution&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">The authors have no conflicts of interest to declare&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11033&#95;108&#95;25088&#95;en&#95;11033&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11033_108_25088_en_11033_t1.jpg" alt="Evolution of laboratory parameters"></img></a></p><p class="elsevierStylePara">Table 1&#46; 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Acute renal failure secondary to sodium and water depletion due to diarrhoea plus acetazolamide
Fracaso renal agudo secundario a depleción hidrosalina por diarrea más acetazolamida
M.. Polaina Rusilloa, J.. Borrego Hinojosaa, A.. Liébana Cañadaa
a Servicio de Nefrología, Complejo Hospitalario de Jaén,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44; </span></p><p class="elsevierStylePara">The use of acetazolamide for the treatment of Meniere&#8217;s syndrome<span class="elsevierStyleSup">1&#44;2</span> is uncommon&#44; since other drugs constitute the first line used in the treatment of this pathology&#46;</p><p class="elsevierStylePara">Here we present the case of a 70-year old woman whose most relevant background involved Meniere&#8217;s syndrome&#44; currently treated with acetazolamide at 250mg&#47;12h with oral potassium supplements&#46;</p><p class="elsevierStylePara">The patient was referred to us due to severe renal failure &#40;urea&#58; 194mg&#47;dl&#59; C-reactive protein&#58; 8&#46;1mg&#47;dl&#41;&#44; with extremely severe metabolic acidosis &#40;venous gas&#58; pH&#58; 7&#46;1&#44; bicarbonate&#58; 6&#46;5mmol&#47;l&#44; PCO<span class="elsevierStyleInf">2</span>&#58; 18mm Hg&#44; PO<span class="elsevierStyleInf">2</span>&#58; 69mm Hg&#41; and anuria&#46; Laboratory analyses from a few months prior indicated C-reactive protein of 1mg&#47;dl&#46; The patient had been admitted to the nearest reference hospital 24 hours before as a result of severe diarrhoea&#44; and continued taking the normal treatment&#46; Hydration treatment had been started without diuresis&#44; and the patient was transferred for monitoring&#46; Upon hospitalisation&#44; dehydration signs were present&#44; with a blood pressure of 80&#47;50mm Hg&#44; anuria&#44; and no fever&#46; At this point the patient did not have diarrhoea&#46;</p><p class="elsevierStylePara">Laboratory analysis revealed acidosis&#44; hypokalaemia &#40;K&#58; 2&#46;9mEq&#47;l&#41; and renal failure similar to that described&#46; We continued to provide intense rehydration therapy&#44; despite which the patient continued with anuria for 24 hours more&#44; with C-reactive protein levels reaching 11mg&#47;dl&#46; Once the volume level was normalised&#44; diuresis started to improve&#44; with clinical and laboratory improvements until reaching a C-reactive protein of 1&#46;2mg&#47;dl upon discharge&#44; with a complete acid-base correction&#46; The evolution of the laboratory values are shown in Table 1&#46;</p><p class="elsevierStylePara">The patient was discharged with the diagnosis of prerenal acute renal failure due to severe hydrosaline depletion&#46; Metabolic acidosis with a normal anion-gap&#44; in the context of acute renal failure due to the ingestion of acetazolamide and diarrhoea&#46;</p><p class="elsevierStylePara">Metabolic acidosis is defined as a process in which the blood pH decreases&#44; with the first effect of decreased bicarbonate concentrations followed by the secondary effect of reduced PCO<span class="elsevierStyleInf">2</span>&#46; Our patient was admitted with acidosis&#58; a pH of 7&#46;1 and a bicarbonate level of 6mEq&#47;l&#46; The acidaemia caused increased ventilation that induced a hypocapnic response that tends to normalise pH&#46; The level of compensation expected can be deduced from the following formula&#58; pCO<span class="elsevierStyleInf">2 </span>&#61; 1&#46;5 &#91;HCO<span class="elsevierStyleInf">3</span>&#93; &#43; 8 &#40;&#177; 2&#41;&#46; In our patient&#44; the level of compensation was adequate &#40;pCO<span class="elsevierStyleInf">2</span>&#58; 17mm Hg&#41;&#44; and so this was a case of pure metabolic acidosis&#44; with correct respiratory compensation&#46;<span class="elsevierStyleSup">3&#44;4</span></p><p class="elsevierStylePara">The patient&#8217;s anion gap upon hospitalisation was normal&#44; near 12&#46; The cases of metabolic acidosis with a normal anion <span class="elsevierStyleItalic">gap</span> &#40;hyperchloremic&#41; suggest that bicarbonate has been replaced by chlorine as it is lost&#46; The most common causes of this type of acidosis are gastrointestinal loss through diarrhoea and renal loss which&#44; in our case&#44; were both caused by acetazolamide&#46;</p><p class="elsevierStylePara">The patient had low potassium levels&#44; lost through the faeces&#44; and volume depletion that increase the synthesis of renin and aldosterone&#44; which in turn raises the renal secretion rate of potassium&#44; in this case&#44; upon admission&#44; to 2&#46;9mEq&#47;l despite oral supplements&#46; Instead of acidic urine we can observe urine pH of six or higher because the metabolic acidosis and hypokalaemia increase the renal excretion and synthesis of NH<span class="elsevierStyleInf">4</span><span class="elsevierStyleSup">&#43; </span>and in turn buffers the H<span class="elsevierStyleSup">&#43; </span>and increases urine pH&#46; The fractional excretion of sodium tends to be low &#40;&#60;1&#37;-2&#37;&#41; in patients with gastrointestinal losses of HCO<span class="elsevierStyleInf">3</span>&#44; although this value was high in our patient&#44; without the classic inversion of sodium&#47;potassium in urine samples typical of prerenal conditions due to the combined effects of diarrhoea and diuretics&#46;<span class="elsevierStyleSup">5&#44;6</span></p><p class="elsevierStylePara">In the case that proximal reabsorption of bicarbonate is ineffective due to the use of acetazolamide&#44; which inhibits carbonic anhydrase&#44; bicarbonate losses are produced&#44; such that this molecule escapes from the proximal tubule and reaches the cortical collecting tubule or the distal convoluted tubule&#44; producing reabsorption of sodium and excretion of potassium and hydrogen ions&#46; The low permeability of bicarbonate impedes its reabsorption&#44; which creates a negative potential in the tubular lumen that increases the excretion of potassium and hydrogen ions&#46;</p><p class="elsevierStylePara">With regard to treatment&#44; the correct approach is to treat the diarrhoea&#44; as well as hydrosaline correction in order to halt the perpetuating stimulus of the renin-angiotensin-aldosterone pathway&#44; with the use of bicarbonate in a continuous perfusion and potassium chloride in order to replace the lost potassium&#44; along with the evident removal of the diuretics&#46; In this manner&#44; our patient responded satisfactorily&#44; with an excellent clinical evolution&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">The authors have no conflicts of interest to declare&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11033&#95;108&#95;25088&#95;en&#95;11033&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11033_108_25088_en_11033_t1.jpg" alt="Evolution of laboratory parameters"></img></a></p><p class="elsevierStylePara">Table 1&#46; Evolution of laboratory parameters</p>"
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