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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44;</span></p><p class="elsevierStylePara">We present the case of a female patient aged 71 years who was referred to our diabetic nephropathy department in April 2009&#46; Her relevant medical history included high blood pressure and type 2 diabetes mellitus &#40;DM2&#41; for more than 20 years&#44; with various diabetes-related complications &#40;diabetic retinopathy&#41;&#59; hyperuricaemia&#44; dyslipidaemia&#44; history of occasional treatment with non-steroidal anti-inflammatory agents&#44; 7 pregnancies with 7 deliveries and no gestosis&#46; Clinical measurements only revealed single-episode nocturia and significant loss of visual acuity in the right eye&#46; Physical examination was normal&#58; blood pressure 120&#47;60mm Hg&#44; weight 72&#46;3kg and height 1&#46;57m&#46; The patient was being treated with alprazolam&#44; furosemide&#44; carvedilol&#44; valsartan&#44; calcium dobesilate and pravastatin&#46; The patient provided an echocardiogram reading that showed moderate left ventricular hypertrophy&#44; ejection fraction of 80&#37; and grade I diastolic dysfunction&#46; She also provided results from an analysis performed by her health centre &#40;Table 1&#41;&#46;</p><p class="elsevierStylePara">On her second visit in August 2009&#44; she only provided analysis results from June 2009 &#40;Table 1&#41;&#46; In November 2009 on her third visit&#44; the patient provided a more recent analytical test &#40;Table 1&#41; and an abdominal ultrasound&#44; which showed a right kidney measuring 9&#46;7cm and a left kidney measuring 9&#46;4cm&#46; Both presented good cortical&#47;medullary differentiation&#46; The patient stated that she had not brought the entire 24 hour urine output sample but that she did not have polydipsia&#46; Since the patient presented hypernatraemia and polyuria&#44; we requested a cerebral MRI without gadolinium&#46; This test&#44; evaluated in January 2010&#44; showed a rounded expanding mass measuring 4cm compatible with parasagittal parietal meningioma in the right convexity&#44; with no perilesional oedema and preserved meningeal<span class="elsevierStyleBold"> </span>grooves&#46; The patient was referred to the neurosurgery division and underwent medial craniotomy in April 2010 to remove bone infiltrated by tumour cells and have it replaced with a titanium mesh&#46; Diagnosis based on histological results was WHO grade I fibrous meningioma with focal bone infiltration&#46; After being referred to the neurosurgery division&#44; the patient did not make follow-up visits until she came in for an appointment in February 2011 in good general health and with improved visual acuity in the right eye&#46; Her most recent evaluation was in August 2011&#59; the patient remained asymptomatic&#44; with no dysnatraemia and a slightly improved glomerular filtration rate &#40;Table 1&#41;&#46;</p><p class="elsevierStylePara">To resume&#44; the patient had stage 3 chronic kidney disease &#40;CKD&#41;&#44; probably secondary to nephroangiosclerosis&#46; On a single occasion during her follow-up period she presented with hypernatraemia&#44; polyuria and euvolaemia&#44; which led to a diagnosis of meningioma&#44; and the tumour was subsequently resected&#46; The differential diagnosis focused on the presence of hypernatraemia with normal total sodium levels&#46; This would also include differential diagnosis for central diabetes insipidus or partial diabetes insipidus with hypodipsia&#46;<span class="elsevierStyleSup">1</span> The absence of polydipsia almost ruled out the diagnoses of diabetes insipidus or primary polydipsia&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">Hypodipsia-hyponatraemia syndrome is characterised by persistent hypernatraemia that cannot be explained by loss of volume&#44; absence of thirst&#44; partial diabetes insipidus&#44; and normal renal response to vasopresin&#46;<span class="elsevierStyleSup">2</span> Causes related to this syndrome are listed in Table 2&#46; Its physiopathology seems to be related to an osmoreceptor disorder that makes these patients dilute and concentrate urine at inappropriately high levels of plasma osmolality&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">The most frequent type of dysnatraemia in patients with CRF and type 2 DM is pseudohyponatraemia secondary to hyperglycaemia or hypertriglyceridaemia&#59; in CFR patients&#44; hyponatraemia is usually much more common than hypernatraemia&#46;<span class="elsevierStyleSup">4-5</span> For that reason&#44; in a patient with CRF and type 2 DM the presence of hypernatraemia&#44; even on a single occasion&#44; requires assessment and a differential diagnosis&#46; The absence of polydipsia made us suspect the presence of hypodipsia-hypernatraemia syndrome&#44; and we were able to identify and correct its cause&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors affirm that they have no conflicts of interest related to the content of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11208&#95;19157&#95;29371&#95;en&#95;t1&#95;10&#46;11208&#46;jpg" class="elsevierStyleCrossRefs"><img src="11208_19157_29371_en_t1_10.11208.jpg" alt="Evolution of patient&#191;s laboratory data"></img></a></p><p class="elsevierStylePara">Table 1&#46; Evolution of patient&#191;s laboratory data</p><p class="elsevierStylePara"><a href="grande&#47;11208&#95;16025&#95;29372&#95;en&#95;t2&#95;10&#46;11208&#46;jpg" class="elsevierStyleCrossRefs"><img src="11208_16025_29372_en_t2_10.11208.jpg" alt="Causes of hypernatraemia syndrome with hypodipsia"></img></a></p><p class="elsevierStylePara">Table 2&#46; Causes of hypernatraemia syndrome with hypodipsia</p>"
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