Abstract: FR-PO0862
Challenging Traditional Hyponatremia Algorithms
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 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
- Mogensen, Jodie Dianne, Baylor College of Medicine, Houston, Texas, United States
- Gregg, Lucile Parker, Michael E DeBakey VA Medical Center, Houston, Texas, United States
- Frost, Livia Ann, Baylor College of Medicine, Houston, Texas, United States
- Shah, Maulin, Baylor College of Medicine, Houston, Texas, United States
- Tucker, Bryan Michael, Baylor College of Medicine, Houston, Texas, United States
Introduction
Traditional US frameworks to diagnose hyponatremia rely on volume status-based algorithms that use subjective physical examination findings and rigid laboratory cutoffs. This inadequately reflects underlying physiology and leads to diagnostic imprecision. We present an adapted physiology-based framework derived from European models (Figure 1), emphasizing objective markers of antidiuretic hormone (ADH) activity and renin-angiotensin-aldosterone system (RAAS) activation. We demonstrate how this approach addresses key diagnostic pitfalls through three cases.
Case Description
Case 1: High serum ethanol levels led to an isoosmolar state in a person with hypotonic hyponatremia. However, the American framework classified this as isoosmolar hyponatremia (differential: pseudohyponatremia). This case highlights the distinction between osmolality and tonicity and that correcting for ineffective osmoles can change diagnostic reasoning.
Case 2: A patient with hypoosmolar hyponatremia due to beer potomania may be considered hypervolemic due to edema (differential: heart failure, cirrhosis, nephrotic syndrome). However, edema can occur in the absence of abnormal effective circulating volume, which is the underlying driver of hyponatremia in such cases. Using urine osmolality as a marker of ADH activity and urine sodium as a marker of RAAS activation provides more useful information to understand the hormonal milieu driving hyponatremia.
Case 3: A patient with metastatic gallbladder cancer presented with hyponatremia from decompensated heart failure and hepatic dysfunction from liver metastasis. Both algorithms may oversimplify such complex cases. Incorporating a physiology-based framework and the full clinical picture could uncover the multiple etiologies contributing to hyponatremia.
Discussion
A diagnostic framework grounded in physiology offers a more robust approach to diagnosing hyponatremia.
Figure 1