Zeki KEMEÇ, Mustafa Adar KEMEÇ
Medical Science and Discovery - 2026;13(9):319-324
Objective: Severe hypercalcemia may cause acute kidney injury (AKI) through volume depletion and alterations in renal vascular function. We present a patient with postsurgical hypoparathyroidism who developed severe hypercalcemia, AKI, hypertension, and transient anemia following inappropriate use of calcitriol and calcium supplementation. Case report : A 44-year-old woman with hypoparathyroidism after total thyroidectomy presented with nausea, vomiting, loss of appetite, and headache. She had been taking calcitriol 4 mug/day, 16 times the prescribed dose, together with 2,000 mg/day elemental calcium and 1,760 IU/day cholecalciferol without medical supervision. On admission, her blood pressure was 160/90 mmHg, serum calcium was 15.4 mg/dL, serum creatinine was 1.23 mg/dL compared with a previous baseline of 0.7 mg/dL, and hemoglobin was 10.3 g/dL. Serum calcium subsequently peaked at 16.9 mg/dL and creatinine at 1.51 mg/dL. No alternative cause of renal dysfunction or a common cause of anemia was identified. Calcitriol and calcium-vitamin D supplementation were discontinued, and intravenous hydration was initiated. Serum calcium and blood pressure normalized by day 4, renal function recovered by day 11, and hemoglobin increased to 12.1 g/dL by day 75 without specific treatment for anemia. Conclusion: Excessive calcitriol and calcium supplementation may result in severe hypercalcemia accompanied by reversible renal dysfunction and other systemic abnormalities. Patients requiring long-term calcium and active vitamin D therapy should undergo regular clinical and biochemical monitoring, particularly when adherence to the prescribed regimen is uncertain. Transient anemia may accompany the acute illness, although its relationship with AKI and hypercalcemia cannot be established from a single case.
