Denosumab boosts bone mineral density but causes marked calcium fluctuations in peritoneal dialysis patient

Patients with end-stage kidney disease (ESKD), particularly those on peritoneal dialysis (PD), frequently suffer from osteoporosis due to complex mineral and bone disorders. Traditional osteoporosis treatments can be challenging in this population due to impaired renal clearance and heightened risk of calcium homeostasis disturbances. Denosumab, a potent inhibitor of bone resorption, is increasingly considered for these patients, but its impact on calcium levels, especially in the context of variable dialysate calcium exposure, remains a significant clinical concern.

This case report details a 56-year-old woman with end-stage kidney disease due to lupus nephritis, on continuous ambulatory PD for 5 years, who presented with severe osteoporosis (lumbar spine 68% and femoral neck 58% of young adult mean [YAM]). She received a single dose of Denosumab 60 mg. To prevent hypocalcemia, dialysate calcium was pre-emptively increased to two 3.5-mEq/L and one 2.5-mEq/L bags daily. Bone mineral density was assessed by dual-energy X-ray absorptiometry (DXA), and serum calcium levels were monitored frequently.

Following Denosumab 60 mg administration, the patient's bone mineral density (BMD) significantly improved within 10 months. Lumbar spine BMD increased from 68% to 78% YAM, and femoral neck BMD rose from 58% to 77% YAM (same facility, identical DXA equipment). Despite pre-emptive dialysate calcium adjustments, symptomatic hypocalcemia developed, reaching a nadir of 7.8 mg/dL on day 7. This necessitated escalation of therapy to three 3.5-mEq/L dialysate bags daily, along with intensified vitamin D and calcium supplementation. This aggressive management subsequently led to an overshoot, with serum calcium peaking at 13.8 mg/dL on day 29. Therapy was then de-escalated, and calcium levels eventually stabilized. This case highlights the precarious balance of calcium management:

Concurrent escalation of dialysate calcium, vitamin D therapy, and calcium supplementation can precipitate overshoot hypercalcemia, even after initial hypocalcemia.