Abstract: TH-PO226
Hyperparathyroidism as a Cause of Low Calcium Requirement during Regional Citrate Anticoagulation: Two Case Reports
Session Information
- Hemodialysis, Hemodiafiltration, and Frequent Dialysis
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 801 Dialysis: Hemodialysis and Frequent Dialysis
Authors
- Afzal, Afsheen, Weill Cornell Medicine, New York, New York, United States
- Liu, Frank, Rogosin Institute, New York, New York, United States
Introduction
CRRT with regional citrate anticoagulation (c-CRRT) relies on a predictable calcium (Ca) balance between effluent removal and Ca replacement to maintain a stable physiologic peripheral ionized Ca (iCa). Our c-CRRT protocol utilizes Ca gluconate for replacement targeting peripheral iCa of 1.05-1.25 mmol/L. In our experience, the majority of patients require 1-2 g/hr of Ca gluconate with variation due primarily to effluent volume. Patients who have unusually low Ca requirements are in negative Ca balance, which can lead to significant demineralization of bone. Existing literature has centered on immobility hypercalcemia as the cause of unusually low Ca requirements during c-CRRT. We present 2 cases of unusually low Ca requirements due to hyperparathyroidism (HPT), which normalized after initiating cinacalcet.
Case Description
Case 1: A 44-year-old male with history of ESKD on hemodialysis (HD) and atrial fibrillation was admitted
with cardiogenic/septic shock requiring c-CRRT. His pre-CRRT peripheral iCa was 1.26 mmol/L. He was noted to have unusually low Ca gluconate requirements (400 mg/hour). Subsequent workup revealed an elevated parathyroid hormone (PTH) level of 867 pg/ml. He was started on cinacalcet 30 mg daily; effluent volume was not changed. By 24h after the first dose, his Ca requirement had increased, with stabilization at 1.3 g/hr by 36h.
Case 2: A 71-year-old male with history of ESKD on HD, coronary artery disease, and congestive heart
failure was admitted with septic shock. His pre-CRRT peripheral iCa was 1.42 mmol/L; hypercalcemia workup was not done at that time. He was noted to have a low Ca gluconate requirement (as low as 400 mg/hr) on c-CRRT. PTH was elevated at 499 pg/ml in spite of systemic hypercalcemia (iCa 1.3 mmol/L). Cinacalcet 30 mg twice daily was initiated; effluent volume was not changed significantly. After 2 doses of cinacalcet, his Ca requirement increased, with eventual stabilization at 1.3-1.4 g/hr by 48h after cinacalcet start.
Discussion
These cases suggest that in addition to immobilization-induced hypercalcemia, HPT should be considered as a cause of hypercalcemia and unexpectedly low Ca requirements in critically ill ESKD patients on c-CRRT. In such patients, treatment of the underlying HPT with cinacalcet can minimize negative Ca balance and subsequent detrimental bone effects while on c-CRRT.