An unusual cause of acute renal failure in a patient with surgical hypoparathyroidism: nephrocalcinosis
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LETTER TO THE EDITOR
An unusual cause of acute renal failure in a patient with surgical hypoparathyroidism: nephrocalcinosis Gu¨lay Koc¸ak • Erdem Koc¸ak • Alper Azak ¨ nverdi Hatice U
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Published online: 15 November 2011 Ó Springer Science+Business Media, LLC 2011
To the Editor, Nephrocalcinosis (NC) is a pattern of renal injury characterized by abundant renal tubular and interstitial deposits of calcium phosphate. Best treatment option for NC depends on the cure of the underlying cause, if possible [1]. During the course of NC, prognosis is highly associated with the severity of renal insufficiency, so early diagnosis has the highest priority. Herein, we present a case of acute renal failure due to NC in a patient with surgical hypoparathyroidism. A 35-year-old woman was referred to our hospital because of acute renal failure of unknown etiology. There was no history of hypertension or diabetes and no family history of renal disease. Her past medical history was remarkable for surgical hypoparathyroidism and hypothyroidism. She had been treated with levothyroxin 50 lg/day, calcitriol 0.5 mcg/day and calcium carbonate 2,500 mg/ day for 15 years. Three months before admission, a routine medical evaluation at a local hospital documented that creatinine level was 0.8 mg/dl. Physical examination did not reveal any pathology. Laboratory tests were as follows: blood urea nitrogen (BUN) 23 mg/dl, creatinine
G. Koc¸ak A. Azak Department of Nephrology, Ankara Education and Research Hospital, Ankara, Turkey E. Koc¸ak (&) Department of Gastroenterology, Ankara Education and Research Hospital, Keklikpınarı mahallesi, 240 sokak, Duru apartmanı, 8/6, Dikmen, C¸ankaya, Ankara, Turkey e-mail: [email protected] ¨ nverdi H. U Department of Pathology, School of Medicine, Ankara University, Ankara, Turkey
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1.94 mg/dl, total calcium 10.7 mg/dl, urinary calcium excretion 740 mg/day, urinary protein 800 mg/day and parathyroid hormone level 4.2 pg/ml (14–72 pg/ml). Urinalysis, arterial blood gas analysis, serum C3 and C4 complement levels were normal. Antinuclear antibody, antineutrophil cytoplasmic antibody, antistreptolysin O, anti-glomerular basement membrane antibody, hepatitis B surface antigen and anti-hepatitis C antibody were all negative. 1,25(OH)2 vitamin D3 and/or 25-OH Vitamin D levels and renal ultrasonography was normal. A renal biopsy was performed which was showed globally sclerosis in 2 of 9 glomeruli on H&E sections, others were normal in size and cellularity. Degenerative changes were found on the tubules characterized by luminal ectasia, irregularity of the luminal contours, and mild degree of interstitial fibrosis. The tubular degenerative changes were accompanied by intraluminal, interstitial basophilic calcifications, consistent with calcium phosphate. The immunofluorescent studies were negative for neither immunoglobulin nor complement. According to laboratory, radiological and pathological findings, NC was diagnosed. Thereafter calcium preparations and calcitriol doses were gradually reduced to a lowe
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