NEPHROLOGY 2004; 9, 89–93 Blackwell Science, LtdOxford, UKNEPNephrology1320-53582004 Asian Pacific Society of NephrologyApril 2004928993Case Report Metastatic calcification and vitamin DN Seyahi et al. Correspondence: Dr Nurhan Seyahi, Halaskargazi c. no: 209–211 d: 2 Huzur ap., Osmanbey, Sisli, Istanbul, Turkey. Email: nseyahi@superonline.com Accepted for publication 11 November 2003. Case Report Intracranial calcification and tumoural calcinosis during vitamin D therapy NURHAN SEYAHI, 1 SUHEYLA APAYDIN, 1 MUZAFFER SARIYAR, 2 KAMIL SERDENGEÇTI 1 and EKREM EREK 1 Departments of 1 Nephrology and 2 General Surgery, Istanbul University, Cerrahpasa Medical Faculty, Istanbul, Turkey SUMMARY: Extraskeletal calcifications are frequently observed in patients with chronic renal failure. However, clinically, they usually remain silent. In this report, we describe two patients with massive extraskeletal calcifications that caused significant morbidity. The first patient had tumoural calcification located on the shoulder and the second patient had severe neurological symptoms caused by intrac- ranial calcifications. High calcium phosphorus product and severe secondary hyperparathyroidism were present in both patients. Furthermore, they both received inappropriately high doses of active vitamin D, even though they failed to respond to this therapy. We suggest to monitor closely the cal- cium, phosphorus and parathyroid hormone levels during calcitriol therapy and to perform parathy- roidectomy, without delay, in patients who were resistant to calcitriol. KEY WORDS: chronic renal failure, intracranial calcification, tumoural calcinosis, vitamin D. INTRODUCTION Extraskeletal (or ‘soft tissue’) calcifications are a frequent and well-known complication in patients with chronic renal failure. 1 In a minority of patients, they can cause significant morbidity and may even become life threat- ening. 2 Recently, their prominent role in cardiovascular morbidity and mortality has also been recognized. 3 In this report, we describe two patients with severe second- ary hyperparathyroidism with unusual soft tissue calcifications. The first patient was presented with tumoural calcification involving the right shoulder and the second case was presented with diffuse intracranial calcification. CASE 1 A 45-year-old male patient had been on regular haemo- dialysis (HD) treatment since 1993. The definite cause of his renal failure was unknown. Bicarbonate dialysis was carried out three times a week for a total of 12 h. During the course of his therapy, he used calcium containing phosphorus binders. In the first 2 years of therapy, he also used aluminium containing phosphorus binders. At the start of HD treatment, a mild secondary hyperparatyroid- ism (intact parathyroid hormone (PTH) 355 pg/mL; normal range 12–72 pg/mL) was detected. Intravenous calcitriol was prescribed and administrated in a pulse reg- imen. Up to 6 mg calcitriol was used per week to obtain acceptable control of PTH levels (<250 pg/mL). How- ever, after April 1998, hyperparathyroidism became more evident, despite calcitriol therapy. Poorly controlled calcium phosphorus product (Ca ¥ P) did not allow the appropriate use of calcitriol. Therefore, mild to moderate hyperparathyroidism was often observed in regular labo- ratory assessments. In February 2001, the patient had started to suffer first from pruritus and then from occasional right shoulder pain, which initially responded well to colchicine and low dose steroid therapy. His biochemical serum data were as follows: calcium 9.3 mg/dL, phosphorus 6.2 mg/dL and PTH 740 pg/mL. By May 2001, he noticed a swelling in his right shoulder. Swelling and pain increased progres- sively over the course of the following 8 months. During this period, hyperparathyroidism became severe, and up to 18 mg/dL calcitriol per week was used. In September