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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44; </span></p><p class="elsevierStylePara">The increase of adynamic bone disease in haemodialysis &#40;HD&#41; patients can hinder the diagnosis of other diseases that progress with latent hypercalcaemia&#46; Here we present a n elusive relevant case&#46;</p><p class="elsevierStylePara">A male patient of 73 years with terminal renal failure &#40;TRF&#41; secondary to diabetic nephropathy that started HD in June 2008&#46; The patient smoked 10 cigarettes&#47;day&#44; and did not consume alcohol&#46; The patient had long-term arterial hypertension &#40;AHT&#41;&#44; type 2 diabetes mellitus for 45 years on treatment with insulin&#44; diabetic retinopathy&#44; dyslipidaemia&#44; chronic ischaemic heart disease tending towards acute myocardial infarction &#40;AMI&#41;&#44; stage III b-IV chronic ischaemia of the lower limbs requiring femoropopliteal bypass in December 2009&#44; 80&#37; stenosis of the left carotid artery&#44; widespread vascular calcifications&#44; chronic bronchopathy&#44; obstructive sleep-apnoea syndrome&#44; small &#40;lacunar infarcts of the thalamus and hemiprotuberance&#41; and large &#40;previous stroke in the left hemisphere&#41; vessel ischaemic brain disease&#44; and polyarthrosis with severe degeneration of the lumbar spinal column&#46;</p><p class="elsevierStylePara">Three years before starting HD&#44; and with treatment including thiazide and oral calcitriol&#44; the patient was hospitalised for severe hypercalcaemia &#40;13&#46;5mg&#47;dl&#41;&#44; with neurological and digestive symptoms&#46; In the subsequent analysis&#44; we observed hilar lymph nodes of a non-pathological size and isolated reticular pulmonary parenchymal opacities&#44; homogeneous hepatosplenomegaly&#44; angiotensin-converting enzyme &#40;ACE&#41; on the upper limit of its normal range &#40;three measurements taken between 30U&#47;l and 60U&#47;l&#44; under normal conditions&#44; normal range&#58; 8-55&#41;&#46; All other tests were negative&#44; and the patient was diagnosed with exogenous intoxication by vitamin D and thiazide&#44; and was treated with parenteral pamidronate&#44; with an excellent clinical evolution and no levels of 1&#44;25 &#40;OH&#41;<span class="elsevierStyleInf">2</span> vitamin D&#46; Since then&#44; the patient has been asymptomatic&#44; with suppressed intact parathyroid hormone &#40;iPTH&#41; levels and a spontaneous tendency towards hypercalcaemia&#44; for which he was diagnosed with adynamic bone disease &#40;ABD&#41;&#46; During the month of July 2009&#44; the patient suffered a progressive condition of asthenia&#44; anorexia&#44; night sweating&#44; disorientation&#44; irritability&#44; amnesic alterations&#44; apathy&#44; apraxia&#44; and motor difficulty for walking&#46; We also observed cortico-subcortical atrophy&#44; leukoaraiosis&#44; and dilation of the ventricular system&#44; and after performing a lumbar puncture with negative biochemical and microbiological results&#44; we ruled out normotensive hydrocephalus&#44; infectious disease&#44; and degeneration of the central nervous system &#40;CNS&#41;&#46; The patient&#8217;s symptoms were explained by small-vessel encephalopathy and a conservative treatment plan&#44; evolving slowly towards chronicity&#46; We did not administer oral calcium&#44; vitamin D&#44; or its derivatives&#44; with dialysis provided with a calcium bath at 2&#46;5mEq&#47;l&#46; In May 2010 the patient had no clinical variations&#44; with hypercalcaemia at maximum values of 12&#46;2mg&#47;dl and iPTH at 6pg&#47;ml &#40;Figure 1&#41;&#46; We performed a complementary study with the following results&#58; normal thyroid profile&#44; negative Mantoux &#40;negative Booster&#41;&#44; chest x-ray indicative of chronic obstructive pulmonary disease &#40;COPD&#41;&#44; normal levels of parathyroid hormone-related peptide &#40;PTHrP&#41;&#44; normal alkaline phosphatase levels&#44; levels of 1&#44;25 &#40;OH&#41;<span class="elsevierStyleInf">2</span> vitamin D reduced to 10pg&#47;ml&#44; normal plasma protein immunoelectrophoresis and proteinogram&#44; negative immunology&#44; bone scan and imaging demonstrated osteopaenia and vascular calcifications with no indications of osteolysis&#44; normal tumour markers&#44; and ACE at 157U&#47;l&#46; The full-body computed tomography &#40;CT&#41; showed several bilateral mediastinal hilar lymph nodes &#40;Figure 2&#41;&#46; Pulmonary fields had ground glass densities with nodular morphology in the middle lobe&#44; periportal&#44; perigastric lymph nodes and in the celiac trunk and left para-aortic and interaortocaval spaces&#44; and spirometry with mixed ventilation abnormalities that were mostly restrictive in nature&#46;</p><p class="elsevierStylePara">We detected bronchitis and chondritis in the bronchoscopy&#46; We then performed a bronchoalveolar lavage and mediastinal fine-needle aspiration with negative cytology for malignancy and no granulomas or lymphoid cellularity&#46; The culture for mycobacteria also resulted negative&#46; The lymphocytic sub-populations in the outflow from the lavage were within normal ranges&#44; with a CD4&#47;CD8 index of 2&#46;22&#46;</p><p class="elsevierStylePara">Diagnosed with pulmonary sarcoidosis&#44; the patient was treated with oral prednisone at 10mg&#47;day for three months with a progressively descending dose until reaching 5mg&#47;48 hours as a maintenance dose&#44; which was sustained for 18 months&#46; The clinical evolution and progress of laboratory parameters &#40;ACE of 36U&#47;l in September 2010&#41; were satisfactory&#59; the patient had improved cognitive state and increased iPTH levels&#44; with normalised hypercalcaemia&#46; The patient is currently on an HD regimen&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Multiple causes can explain hypercalcaemia in a patient on HD &#40;the use of calcium chelating agents&#44; dialysed with a high-calcium bath&#44; use of vitamin D and derivatives&#44; poorly controlled secondary hyperthyroidism&#44; ABD&#44; and osteomalacia&#41;&#46;&#160; One uncommon cause is sarcoidosis&#44; a granulomatous disease of unknown origin&#44; in which an extra-renal synthesis of calcitriol is produced by activated macrophages&#46;<span class="elsevierStyleSup">1 </span>The disease normally involves constitutional symptoms &#40;weight loss&#44; fever&#41;&#44; arthralgia&#44; asthenia&#44; and pulmonary symptoms &#40;reticular opacities and bilateral pulmonary hilar lymph node&#41;&#46; It tends to respond to corticosteroid therapy that should be maintained for at least one year&#46; Extra-thoracic symptoms occur in only 30&#37; of cases&#46; Cases mentioned in HD patients are rare in the medical literature<span class="elsevierStyleSup">2-5</span> and tend to be diagnosed based on hypercalcaemia with systemic and pulmonary symptoms&#46; Our patient had increased ACE levels &#40;75&#37;&#41;&#44; neurological symptoms &#40;5&#37;&#41;&#44; hepatosplenomegaly &#40;20&#37;-25&#37;&#41;&#44; and hypercalcaemia &#40;10&#37;-20&#37;&#41;&#46; We had previously observed reticular pulmonary opacities&#44; with no increase in ACE levels or symptoms in other areas that would suggest this diagnosis&#46; Additionally&#44; the patient&#44; being diabetic&#44; had widespread calcifications and multiple risk factors that could explain the vascular encephalopathy&#59; the chronic pneumopathy had already been considered as ABD&#46; The patient&#8217;s clinical evolution was latent and progressive&#44; with no elevations in ACE levels or true hypercalcaemia until three years after the first crisis&#46; The non-specific constitutional symptoms and the sum of causes that all could have explained the patient&#8217;s condition hindered making the proper diagnosis&#46; After treatment&#44; iPTH levels were stable between 180pg&#47;m and 270pg&#47;m&#44; which was surprising&#46; We also want to bring attention to the fact that cases of hypercalcaemia right on the limit are not always due to ABD&#44; which we believe to be adequate reason to consider other possible diagnoses when the circumstances call for it&#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;10974&#95;16025&#95;25077&#95;en&#95;f1&#95;10974&#46;jpg" class="elsevierStyleCrossRefs"><img src="10974_16025_25077_en_f1_10974.jpg" alt="Evolution of calcium&#44; phosphorous and intact parathyroid hormone &#40;iPTH&#41; levels"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Evolution of calcium&#44; phosphorous and intact parathyroid hormone &#40;iPTH&#41; levels</p><p class="elsevierStylePara"><a href="grande&#47;10974&#95;108&#95;25078&#95;en&#95;10974&#95;f2&#46;jpg" class="elsevierStyleCrossRefs"><img src="10974_108_25078_en_10974_f2.jpg" alt="Chest computed tomography&#46; Hilar lymph nodes"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Chest computed tomography&#46; Hilar lymph nodes</p>"
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