Abstract: SA-PO0622
The Cryptic Correlation of Hypercalcemia with Adrenal Insufficiency
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
- Kurian, James, Baylor College of Medicine, Houston, Texas, United States
- Shah, Maulin, Baylor College of Medicine, Houston, Texas, United States
- Holliday, Michael Wayne, Baylor College of Medicine, Houston, Texas, United States
- Win, Shwe Yee, Baylor College of Medicine, Houston, Texas, United States
Group or Team Name
- Baylor Nephrology
Introduction
Adrenal insufficiency (AI) is a rare but well-documented cause of parathyroid hormone (PTH)-independent hypercalcemia that is likely under-recognized in clinical practice. We present a case highlighting this association and its diagnostic implications.
Case Description
A 79-year-old male with past medical history significant for stage 4 chronic kidney disease, and idiopathic pulmonary fibrosis presented after a fall. He was admitted two months earlier following a similar episode and found to have orthostatic hypotension, and was discharged on midodrine. Laboratory evaluation revealed worsening hyponatremia (126 mEq/L) and borderline hypercalcemia (10.2 mg/dL). Isotonic saline administration resulted in further decline in serum sodium without improvement in calcium levels. Serum and urine protein electrophoreses were negative. Inactive and active levels of serum vitamin D were normal. Intact PTH level was appropriately low, but adrenocorticotropic hormone levels were high. Following an inappropriately low morning, fasting cortisol level, failure to respond to exogenous ACTH treatment established a diagnosis of primary AI. Treatment with hydrocortisone resulted in normalization of serum sodium and calcium levels.
Discussion
The pathophysiology of hypercalcemia in AI is poorly understood. A likely major contributor is hypovolemia that results in increased urinary calcium reabsorption. Additionally, hypercalcemia may occur from vitamin D dysregulation, as ACTH and cortisol have regulatory effects on alpha-1-hydroxylase. Hypercalemia may persist in AI even in euvolemic patients with controlled diets, and although the underlying mechanisms are unclear, bone likely serves as a reservoir for calcium release. Bone resorption with calcium release appears to be PTH-independent, and bone biopsies in these patients have not shown increased osteoclast activity. Fortunately, standard treatment of AI typically leads to resolution of hypercalcemia. Clinicians should be aware of hypercalcemia from AI as it may help in earlier diagnosis and management of the condition.
Figure 1