Journal of Advances in Medicine and Medical Research

We report the 1^st case of severe, symptomatic hypocalcemia after denosumab (RANKL inhibitor) treatment in a peritoneal dialysis patient with secondary hyperparathyroidism and osteoporosis. A 58-year-old Caucasian female has been receiving chronic ambulatory peritoneal dialysis for four years secondary to polycystic kidney disease. Laboratory studies revealed: albumin-corrected calcium 9.0 mg/dL, phosphorus 5 mg/dL, alkaline phosphatase (ALP) 58 U/L [normal, 40-105], albumin 3.4 gm/dL [normal, 3.6-5.4] and intact parathyroid hormone (PTH) 315 pg/mL [normal, 40-72]. Marked osteoporosis was noted on the DXA scan, preventing her from renal transplantation considerations. She had failed conventional medical treatment, including per os calcium, monthly ergocalciferol (50,000 units/month), activated vitamin-D analog (doxercalciferol) and renal-failure adjusted alendronate (70 mg twice a month). She was started on subcutaneous denosumab 60 mg every 6 months. After her first dose, she developed a progressive drop of calcium, phosphorus, bicarbonate and magnesium, in spite of massive escalation of doxercalciferol and calcium supplementation. Hypocalcemia nadired at 6.3 mg/dL with symptomatic tetany, requiring a brief hospitalization approximately 7 weeks after denosumab treatment. Her elevated PTH rose further transiently (647 pg/mL), along with ALP (123 U/L). Bone-mineral parameters normalized approximately 3 months after denosumab administration. The observed phenomenon resembled the phenotype of “hungry bone syndrome” observed after surgical parathyroidectomy.
Conclusion: Treatment decisions based on bone densitometry results alone are not transposable between patients with or without end-stage renal disease. Denosumab may lead to critical hypocalcemia in dialysis patients and further aggravate existing secondary hyperparathyroidism.