Abstract: SA-PO0626
Acute Hypercalcemia After Calcium Sulfate Antibiotic Bead Placement in a Patient with CKD
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Hobeika, Natalie, Northwestern Memorial HealthCare, Chicago, Illinois, United States
- Tuazon, Jennifer A., Northwestern Memorial HealthCare, Chicago, Illinois, United States
Introduction
Antibiotic-eluting calcium sulfate beads are increasingly used in orthopedic surgery for local infection control. Symptomatic hypercalcemia is a rare but potentially life-threatening complication, reported in fewer than 1% of cases in large series. Patients with chronic kidney disease (CKD) may be particularly vulnerable due to impaired renal calcium excretion. We report severe hypercalcemia with acute kidney injury (AKI) following calcium sulfate bead placement in a patient with CKD stage 3.
Case Description
An 88-year-old man with CKD stage 3 (baseline eGFR 40-50 mL/min, creatinine 1.0-1.2 mg/dL) presented with altered mental status three days after incision and drainage of a right hip surgical site infection following fixation of a periprosthetic femoral fracture. Calcium sulfate beads containing vancomycin (1 g) and tobramycin (1.2 g) were placed intraoperatively.
Labs revealed severe hypercalcemia (peak calcium 14.9 mg/dL, from 9.5 mg/dL two days prior) and AKI (creatinine 2.39 mg/dL, from 1.30 mg/dL). Workup showed suppressed PTH (18 pg/mL), low 25-hydroxyvitamin D (17.5 ng/mL), undetectable 1,25-dihydroxyvitamin D (< 8 pg/mL), normal PTHrP (10 pg/mL), and normal phosphorus (3.9 mg/dL), consistent with non-PTH-mediated hypercalcemia. Treatment with isotonic saline, calcitonin, and pamidronate led to improvement in calcium and renal function.
Discussion
This case illustrates calcium sulfate antibiotic beads as an underrecognized iatrogenic cause of acute hypercalcemia. The temporal relationship between bead placement and the rapid calcium rise, combined with suppressed PTH, normal PTHrP, and low vitamin D metabolites, supports systemic calcium absorption from dissolving beads as the primary mechanism. Postoperative immobilization and dehydration likely compounded the severity, consistent with prior reports identifying renal impairment and immobility as key risk factors. This case underscores the importance of considering recent procedural exposures in acute non-PTH-mediated hypercalcemia.
Figure 1: Serum calcium levels (mg/dL) over a 10-day postoperative period