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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleItalic">Dear Editor&#44; </span></p><p class="elsevierStylePara"> Hypercalcaemic crisis is a rare form of presentation of primary hyperparathyroidism&#46; Only small case series have been reported in the literature &#40;1&#44;2&#41;&#46; It is characterised by severe hypercalcaemia&#44; renal failure and an altered state of consciousness&#46; We present the case of a 70-year-old patient&#44; who was admitted for acute kidney injury caused by a hypercalcaemic crisis within the context of previously undetected primary hyperparathyroidism&#46; The therapeutic approach and patient progress are discussed&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Clinical Case </span></p><p class="elsevierStylePara"> The patient is a 70-year-old white male with a history of benign prostatic hyperplasia&#44; recurrent atrial fibrillation and right hemithyroidectomy due to nodular hyperplasia&#44; as well as chronic kidney disease that had not been studied &#40;baseline creatinine 1&#46;5 mg&#47;dL&#41;&#46;</p><p class="elsevierStylePara"> He was admitted to the emergency room due to symptoms that included unsteady gait and generalized weakness&#44; which had been progressing in the last three months and for which the patient had been previously treated at another hospital&#46; Upon physical examination&#44; the patient was dehydrated&#44; confused&#44; bradypsychic&#44; and presented distal tremor&#46;</p><p class="elsevierStylePara"> Table 1 summarizes the laboratory data&#44; which highlight a significant deterioration in renal function&#44; severe hypercalcaemia and marked increase in PTH levels &#40;20 times the laboratory reference value&#41;&#46; Treatment was initiated with IV fluid therapy&#44; infusion of furosemide&#44; and intravenous corticosteroids&#44; bisphosphonates and calcitonin&#46; Due to the severity of the neurological symptoms&#44; urgent simultaneous renal replacement therapy was indicated by means of haemodialysis with low calcium dialysate&#46; The patient showed temporary clinical improvement&#44; but&#44; due to the persistent renal failure and rebound hypercalcaemia &#40;increase in blood calcium level &#62; 2 mg&#47;dL 24 hours post-haemodialysis&#41;&#44; continued daily session were required&#46;</p><p class="elsevierStylePara"><img alt="Table I – Baseline and progressive laboratory data" src="498v35n02-90412449fig1.jpg"></img></p><p class="elsevierStylePara"> The etiologic study ruled out myeloproliferative processes and other neoplasms &#40;no monoclonal component in the protein analysis&#59; negative Bence-Jones proteinuria&#41;&#44; infectious disease &#40;nonreactive serology&#41; and autoimmune diseases&#46; Renal ultrasound demonstrated normal-sized kidneys and good cortico-medullary differentiation&#46; The thoracic-abdominal CT scan showed a retroesophageal mass measuring 5&#46;6 &#215; 3&#46;2 &#215; 6&#46;8 cm&#44; which was suspicious for parathyroid tumour&#44; in addition to bilateral hypodense adrenal nodules&#58; right 27 &#215; 18 mm and left 15 &#215; 11 mm&#46; Parathyroid scintigraphy confirmed the image &#40;Figure 1A&#41;&#46;</p><p class="elsevierStylePara"><img alt="Figure 1 – Parathyroid scintigraphy with Tc 99m-sestamibi&#59; B&#41; Surgical piece&#59; C&#41; Histology of parathyroid adenoma " src="498v35n02-90412449fig2.jpg"></img></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Figure 1 &#8211; Parathyroid scintigraphy with Tc 99m-sestamibi&#59; B&#41; Surgical piece&#59; C&#41; Histology of parathyroid adenoma </span></p><p class="elsevierStylePara"> The Endocrinology Unit was consulted about these findings&#44; and phaeochromocytoma was ruled out &#40;negative urine catecholamine and metanephrine&#41;&#46; In a joint session with the General Surgery Unit&#44; surgical management was decided upon&#44; which included resection of an 8-cm parathyroid tumour <span class="elsevierStyleBold">&#40;Figure 1B&#41;</span>&#46; The Pathology Unit reported the mass to be a parathyroid adenoma with no capsular or vascular invasion <span class="elsevierStyleBold">&#40;Figure 1C&#41;</span>&#46;</p><p class="elsevierStylePara"> During the immediate post-operative period&#44; the patient developed &#8220;hungry bone syndrome&#8221; and therefore required intravenous and oral calcium supplementation for severe hypocalcaemia as well as daily haemodialysis sessions until nine days after the surgery&#46;</p><p class="elsevierStylePara"> Nine months later&#44; the patient is asymptomatic&#44; with calcaemia within normal limits and no need for supplements as well as partial recovery of renal function &#40;creatinine 2&#46;7 mg&#47; dL&#44; <span class="elsevierStyleBold">Figure 2</span>&#41;&#46; It should be noted that renal function is still altered one year after the surgery&#44; despite calcaemia normalization&#46;</p><p class="elsevierStylePara"><img alt="Figure 2 – Progress of calcaemia and renal function" src="498v35n02-90412449fig3.jpg"></img></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Figure 2 &#8211; Progress of calcaemia and renal function</span></p><p class="elsevierStylePara"> The great majority of parathyroid adenomas are asymptomatic&#44; and only a small percentage cause severe hypercalcaemia and renal failure requiring renal replacement therapy &#40;3-4&#41;&#46; A recent and extensive literature review only identified 17 cases of hypercalcaemia &#62; 20 mg&#47;dL&#44; with a mortality rate of 60&#37; &#40;5&#41;&#46; There are only three cases reported with calcaemia &#62; 30 mg&#47;dL &#40;6-8&#41;&#46;</p><p class="elsevierStylePara"> The most relevant aspects in this case report are&#58;</p><p class="elsevierStylePara"> &#8226; The onset of a parathyroid adenoma as severe hypercalcaemia</p><p class="elsevierStylePara"> &#8226; Renal failure secondary to hypercalcaemia crisis that required renal replacement therapy and only partially recovered after correcting the cause of the hypercalcaemia</p><p class="elsevierStylePara"> &#8226; The large size of the parathyroid tumour with non-malignant histology</p><hr></hr><p class="elsevierStylePara"><a href="http&#58;&#47;&#47;dx&#46;doi&#46;org&#47;10&#46;3265&#47;Nefrologia&#46;pre2014&#46;Oct&#46;12780" class="elsevierStyleCrossRefs">http&#58;&#47;&#47;dx&#46;doi&#46;org&#47;10&#46;3265&#47;Nefrologia&#46;pre2014&#46;Oct&#46;12780</a></p><p class="elsevierStylePara"> &#42; <span class="elsevierStyleItalic">Corresponding author</span>&#46;<br></br> Andrea Chac&#243;n&#44; Nephrology&#44; <br></br> Arnau de Vilanova Hospital&#44; Magdalena 33&#44; 25007&#44; <br></br> Lleida&#44; Lleida&#44; Spain&#46; <span class="elsevierStyleItalic">Tel&#46;&#58; </span>622456547 <span class="elsevierStyleItalic"><br></br> E-mail&#58;</span><a href="mailto&#58;mytleya&#64;gmail&#46;com" class="elsevierStyleCrossRefs">mytleya&#64;gmail&#46;com</a></p>"
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Acute kidney injury secondary to very severe hypercalcaemic crisis caused by primary hyperparathyroidism
Fracaso renal agudo secundario a crisis de hipercalcemia muy severa por hiperparatiroidismo primario
Andrea Chacóna, Ana Vilara, David Arroyoa, Felipe Sarróa, Lourdes Cravera, Susana Rosb, Carolina Lópezc, Alex Castillod, Xavier Matías-Guiud, Elvira Fernández-Giráldeza
a Nephrology, Hospital Arnau de Vilanova [Arnau de Vilanova Hospital], Lleida, Lleida (Spain)
b Digestive System and General Surgery, Hospital Arnau de Vilanova, Lleida, Lleida (Spain)
c Endocrinology, Hospital Arnau de Vilanova, Lleida, Lleida (Spain)
d Pathology, Hospital Arnau de Vilanova, Lleida, Lleida (Spain)
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleItalic">Dear Editor&#44; </span></p><p class="elsevierStylePara"> Hypercalcaemic crisis is a rare form of presentation of primary hyperparathyroidism&#46; Only small case series have been reported in the literature &#40;1&#44;2&#41;&#46; It is characterised by severe hypercalcaemia&#44; renal failure and an altered state of consciousness&#46; We present the case of a 70-year-old patient&#44; who was admitted for acute kidney injury caused by a hypercalcaemic crisis within the context of previously undetected primary hyperparathyroidism&#46; The therapeutic approach and patient progress are discussed&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Clinical Case </span></p><p class="elsevierStylePara"> The patient is a 70-year-old white male with a history of benign prostatic hyperplasia&#44; recurrent atrial fibrillation and right hemithyroidectomy due to nodular hyperplasia&#44; as well as chronic kidney disease that had not been studied &#40;baseline creatinine 1&#46;5 mg&#47;dL&#41;&#46;</p><p class="elsevierStylePara"> He was admitted to the emergency room due to symptoms that included unsteady gait and generalized weakness&#44; which had been progressing in the last three months and for which the patient had been previously treated at another hospital&#46; Upon physical examination&#44; the patient was dehydrated&#44; confused&#44; bradypsychic&#44; and presented distal tremor&#46;</p><p class="elsevierStylePara"> Table 1 summarizes the laboratory data&#44; which highlight a significant deterioration in renal function&#44; severe hypercalcaemia and marked increase in PTH levels &#40;20 times the laboratory reference value&#41;&#46; Treatment was initiated with IV fluid therapy&#44; infusion of furosemide&#44; and intravenous corticosteroids&#44; bisphosphonates and calcitonin&#46; Due to the severity of the neurological symptoms&#44; urgent simultaneous renal replacement therapy was indicated by means of haemodialysis with low calcium dialysate&#46; The patient showed temporary clinical improvement&#44; but&#44; due to the persistent renal failure and rebound hypercalcaemia &#40;increase in blood calcium level &#62; 2 mg&#47;dL 24 hours post-haemodialysis&#41;&#44; continued daily session were required&#46;</p><p class="elsevierStylePara"><img alt="Table I – Baseline and progressive laboratory data" src="498v35n02-90412449fig1.jpg"></img></p><p class="elsevierStylePara"> The etiologic study ruled out myeloproliferative processes and other neoplasms &#40;no monoclonal component in the protein analysis&#59; negative Bence-Jones proteinuria&#41;&#44; infectious disease &#40;nonreactive serology&#41; and autoimmune diseases&#46; Renal ultrasound demonstrated normal-sized kidneys and good cortico-medullary differentiation&#46; The thoracic-abdominal CT scan showed a retroesophageal mass measuring 5&#46;6 &#215; 3&#46;2 &#215; 6&#46;8 cm&#44; which was suspicious for parathyroid tumour&#44; in addition to bilateral hypodense adrenal nodules&#58; right 27 &#215; 18 mm and left 15 &#215; 11 mm&#46; Parathyroid scintigraphy confirmed the image &#40;Figure 1A&#41;&#46;</p><p class="elsevierStylePara"><img alt="Figure 1 – Parathyroid scintigraphy with Tc 99m-sestamibi&#59; B&#41; Surgical piece&#59; C&#41; Histology of parathyroid adenoma " src="498v35n02-90412449fig2.jpg"></img></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Figure 1 &#8211; Parathyroid scintigraphy with Tc 99m-sestamibi&#59; B&#41; Surgical piece&#59; C&#41; Histology of parathyroid adenoma </span></p><p class="elsevierStylePara"> The Endocrinology Unit was consulted about these findings&#44; and phaeochromocytoma was ruled out &#40;negative urine catecholamine and metanephrine&#41;&#46; In a joint session with the General Surgery Unit&#44; surgical management was decided upon&#44; which included resection of an 8-cm parathyroid tumour <span class="elsevierStyleBold">&#40;Figure 1B&#41;</span>&#46; The Pathology Unit reported the mass to be a parathyroid adenoma with no capsular or vascular invasion <span class="elsevierStyleBold">&#40;Figure 1C&#41;</span>&#46;</p><p class="elsevierStylePara"> During the immediate post-operative period&#44; the patient developed &#8220;hungry bone syndrome&#8221; and therefore required intravenous and oral calcium supplementation for severe hypocalcaemia as well as daily haemodialysis sessions until nine days after the surgery&#46;</p><p class="elsevierStylePara"> Nine months later&#44; the patient is asymptomatic&#44; with calcaemia within normal limits and no need for supplements as well as partial recovery of renal function &#40;creatinine 2&#46;7 mg&#47; dL&#44; <span class="elsevierStyleBold">Figure 2</span>&#41;&#46; It should be noted that renal function is still altered one year after the surgery&#44; despite calcaemia normalization&#46;</p><p class="elsevierStylePara"><img alt="Figure 2 – Progress of calcaemia and renal function" src="498v35n02-90412449fig3.jpg"></img></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Figure 2 &#8211; Progress of calcaemia and renal function</span></p><p class="elsevierStylePara"> The great majority of parathyroid adenomas are asymptomatic&#44; and only a small percentage cause severe hypercalcaemia and renal failure requiring renal replacement therapy &#40;3-4&#41;&#46; A recent and extensive literature review only identified 17 cases of hypercalcaemia &#62; 20 mg&#47;dL&#44; with a mortality rate of 60&#37; &#40;5&#41;&#46; There are only three cases reported with calcaemia &#62; 30 mg&#47;dL &#40;6-8&#41;&#46;</p><p class="elsevierStylePara"> The most relevant aspects in this case report are&#58;</p><p class="elsevierStylePara"> &#8226; The onset of a parathyroid adenoma as severe hypercalcaemia</p><p class="elsevierStylePara"> &#8226; Renal failure secondary to hypercalcaemia crisis that required renal replacement therapy and only partially recovered after correcting the cause of the hypercalcaemia</p><p class="elsevierStylePara"> &#8226; The large size of the parathyroid tumour with non-malignant histology</p><hr></hr><p class="elsevierStylePara"><a href="http&#58;&#47;&#47;dx&#46;doi&#46;org&#47;10&#46;3265&#47;Nefrologia&#46;pre2014&#46;Oct&#46;12780" class="elsevierStyleCrossRefs">http&#58;&#47;&#47;dx&#46;doi&#46;org&#47;10&#46;3265&#47;Nefrologia&#46;pre2014&#46;Oct&#46;12780</a></p><p class="elsevierStylePara"> &#42; <span class="elsevierStyleItalic">Corresponding author</span>&#46;<br></br> Andrea Chac&#243;n&#44; Nephrology&#44; <br></br> Arnau de Vilanova Hospital&#44; Magdalena 33&#44; 25007&#44; <br></br> Lleida&#44; Lleida&#44; Spain&#46; <span class="elsevierStyleItalic">Tel&#46;&#58; </span>622456547 <span class="elsevierStyleItalic"><br></br> E-mail&#58;</span><a href="mailto&#58;mytleya&#64;gmail&#46;com" class="elsevierStyleCrossRefs">mytleya&#64;gmail&#46;com</a></p>"
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