Abstract: SA-PO0562
Idiopathic Hypercalcemia in Decompensated Cirrhosis
Session Information
- Bones, Stones, and Mineral Metabolism: Research and Cases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Aamer, Sameen, University of Minnesota Medical School, Minneapolis, Minnesota, United States
- Sakamoto, Ayumi Emily, University of Minnesota Medical School, Minneapolis, Minnesota, United States
- Gill, Mannat, University of Minnesota Medical School, Minneapolis, Minnesota, United States
- Koubar, Sahar, University of Minnesota Medical School, Minneapolis, Minnesota, United States
- Thorne, Peter E., University of Minnesota Medical School, Minneapolis, Minnesota, United States
Introduction
Idiopathic non-PTH-mediated hypercalcemia in decompensated cirrhosis is a rare and poorly characterized diagnosis of exclusion. We report two cases illustrating its diagnostic and management challenges.
Case Description
Case 1: A 54-year-old woman with autoimmune hepatitis post liver transplantation, CKD stage 3a, and MGUS presented with decompensated cirrhosis, ascites, hypercalcemia, and acute kidney injury (AKI). Extensive evaluation for hypercalcemia was unremarkable (Table 1). PET scan, CT chest, abdomen, pelvis, and bone marrow biopsy showed no evidence of malignancy or granulomatous disease. Despite intravenous fluids, albumin, calcitonin, denosumab, and empiric prednisone, hypercalcemia remained refractory with progressive renal dysfunction requiring hemodialysis. Serum calcium normalized and kidney function recovered only after repeat liver transplantation.
Case 2: A 66-year-old woman with alcohol-related decompensated cirrhosis was admitted for AKI, developing hypercalcemia during the hospitalization. Workup for common causes of hypercalcemia, including serum protein electrophoresis, was unrevealing (Table 1). Her AKI and hypercalcemia resolved with IV fluids, calcitonin, and zoledronic acid.
Discussion
The proposed mechanisms for idiopathic hypercalcemia in decompensated cirrhosis include systemic inflammation driving osteoclast-mediated bone resorption via TNF, IL-1, and RANKL/OPG dysregulation, and bilirubin-mediated suppression of osteogenic signaling. AKI in decompensated cirrhosis, combined with hypercalcemia-induced renal vasoconstriction, further reduces urinary calcium excretion and may amplify both the severity and persistence of hypercalcemia. Idiopathic hypercalcemia in decompensated cirrhosis is rare with poor prognosis. Prolonged inpatient hypercalcemia independently predicts 90-day mortality, warranting greater familiarity of the condition amongst clinicians.
| Parameter | Case 1 | Case 2 |
| Peak calcium, corrected (8.8-10.4 mg/dL) | 13.1 | 14.2 |
| Peak creatinine (0.51-0.95 mg/dL) | 4.11 | 4.6 |
| PTH (15-65 pg/mL) | 14 | 9 |
| PTHrP (0-3.4 pmol/L) | 3.1 | 3.0 |
| 1,25-OH Vitamin D (19.9-79.3 pg/mL) | 52 | 7 |
| 24 hour urine calcium (0.1-0.3 g/24 Hr) | 0.03 | N/A |
| Peak total bilirubin (less than 1.2 mg/dL) | 5.3 | 4.1 |
Table 1: Select laboratory parameters in two cases of idiopathic hypercalcemia of decompensated cirrhosis