Denosumab increased bone mineral density but caused marked serum calcium fluctuations in a patient undergoing peritoneal dialysis.

Yamada Shunsuke, Enomoto Soma, Matsuo Kana, Sonezaki Yusuke et al. — CEN case reports

Abstract

Denosumab is increasingly used to treat osteoporosis in patients with advanced kidney disease, but clinically significant disturbances in calcium homeostasis remain a major concern. We report a peritoneal dialysis (PD) case in which denosumab administration was followed by pronounced calcium fluctuations requiring medication management. A 56-year-old woman with end-stage kidney disease due to lupus nephritis, receiving prednisolone (5 mg/day), had been on continuous ambulatory PD (1.5-L exchanges three times daily) for 5 years. Baseline intact parathyroid hormone was 176 pg/mL. Osteoporosis was confirmed by dual-energy X-ray absorptiometry (lumbar spine 68% and femoral neck 58% of the young adult mean [YAM]). Denosumab 60 mg was administered, and BMD increased within 10 months to 78% YAM at the lumbar spine and 77% YAM at the femoral neck (same facility, identical DXA equipment). To mitigate hypocalcemia, dialysate calcium was pre-emptively increased to two 3.5-mEq/L and one 2.5-mEq/L bags per day (albumin-corrected calcium 9.5 mg/dL at dosing). Nonetheless, symptomatic hypocalcemia developed (nadir 7.8 mg/dL on day 7), prompting escalation to three 3.5-mEq/L bags with intensified vitamin D therapy and calcium supplementation. Serum calcium then overshot, peaking at 13.8 mg/dL on day 29; therapy was de-escalated and calcium stabilized. This case highlights that while daily dialysate calcium exposure in PD may buffer early hypocalcemia, concurrent escalation of dialysate calcium, vitamin D therapy, and calcium supplementation can precipitate overshoot hypercalcemia. Frequent monitoring and staged, stepwise prescription changes during the first month after denosumab are essential. Standardized PD-specific post-denosumab calcium management protocols are urgently needed.

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