Abstract: TH-PO0228
A Calcium Conundrum: When CKD Isn't the Only Cause of Bone Mineral Disease
Session Information
- Bone and Mineral Metabolism: Clinical Reports and Practice
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Grigsby, Sierrah M, Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Brier, Benjamin E., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Yuan, Christina M., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Blum, Christina L., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
Introduction
Bone mineral disease (BMD) is a common complication of chronic kidney disease (CKD), typically manifesting as secondary hyperparathyroidism (SHPT). As kidney function declines, hypocalcemia, hyperphosphatemia, and compensatory increases in parathyroid hormone (PTHi) occur. This case demonstrates a discordant pattern of hyperparathyroidism not due to SHPT in a patient with advanced CKD. Understanding the SHPT pathophysiology thoroughly is crucial for appropriate diagnosis and management, particularly in the renal transplant candidates.
Case Description
A 65-year-old female with a history of hypertension, stroke, smoking, and type 2 diabetes mellitus was followed for Stage 4 CKD with an estimated glomerular filtration rate (eGFR) of 20 mL/min/1.73m^2. Routine laboratory evaluation revealed a calcium of 10.4 mg/dL, albumin of 4.6 g/dL, phosphorus of 3.9 mg/dL, vitamin D of 51 ng/ml, and PTHi of 407 pg/mL. Her normal calcium and phosphorus, despite a significantly elevated PTHi, deviated from the expected pattern of SHPT in advanced CKD, raising suspicion for primary hyperparathyroidism (PHPT). She was found to have both a 4cm parathyroid adenoma and a remarkably low urinary calcium excretion (6mg/day after oral calcium loading). The presence of adenoma and hypocalciuria suggested her hyperparathyroidism was not due solely to SHPT, and either PHPT or familial hypocalciuric hypocalcemia (FHH) were contributing.
Discussion
Typically, BMD in CKD is characterized by phosphate retention, decreased calcitriol production, and subsequent hypocalcemia, driving PTH secretion. PTHi levels increase when eGFR<60mL/min/1.73m^2. In contrast, PHPT is caused by autonomous PTH secretion leading to hypercalcemia, hypophosphatemia, and hypercalciuria; FHH has a similar biochemical profile but with hypocalciuria. This patient presented with disproportionately elevated PTHi, with normal calcium and phosphorus, prompting further investigation. The case emphasizes the importance of thoroughly evaluating potential underlying conditions, such as occult malignancy or, as here, FHH, and PHPT, in patients with presumed SHPT but an aberrant metabolic profile.