Abstract: FR-PO0622
Hyponatremia Associated with Sjogren Disease
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, 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
- Zhang, Grace Joyce, The University of British Columbia, Vancouver, British Columbia, Canada
- Zhang, Chi, The University of British Columbia Faculty of Medicine, Vancouver, British Columbia, Canada
Introduction
Sjogren’s Disease (SD) is an autoimmune disease affecting the lacrimal and salivary glands, leading to dry eyes and mouth. Other organs may also be affected, including the kidneys, joints, and nervous system. We present a case of hyponatremia and potential inappropriate antidiuretic hormone secretion (SIADH) with SD.
Case Description
A 70 year-old Caucasian woman with history of SD, systemic autoimmune rheumatic disease, fibromyalgia, obstructive sleep apnea, insomnia, and hypothyroidism presents with a fall followed by loss of consciousness. She was found in subzero temperatures and developed hypothermia. She sustained a knee fracture and labs showed hyponatremia, Na+ of 105 mmol/L and hypokalemia, K+ of 2.2 mmol/L. She was taking 50 mcg of levothyroxine and 7.5 mg of mirtazapine daily. Since then, her medical records consistently report hyponatremia. One year later, she was admitted to ICU due to hyponatremia, Na+ of 107 mmol/L, hypokalemia, K+ of 1.8 mmol/L, and post-operative infection following a colectomy due to volvulus. Her urine osmolality was high at 492 mOsm/kg. TSH and cortisol levels were normal. Sodium was corrected with 3% saline and DDAVP clamp protocol. She was advised to take 9g salt tablets per day plus fluid restriction. It was suspected that she has SIADH due to concurrent hyponatremia and high urine osmolality. Two months later, she was still hyponatremic with sodium of 128 mmol/L despite taking salt tablets. Her urine osmolality was relatively high at 320 mOsm/kg. Testing revealed SSA>240 U/mL and SSB>320 U/mL, supporting SD diagnosis. Rheumatoid factor was >120 IU/mL. Her TSH and cortisol levels were normal at 1.59 mU/L and 353 nmol/L, respectively. Her blood pressure was high at 144/84 mmHg. She was prescribed 40 mEq of potassium chloride per day for hypokalemia and 5 mg of amlodipine per day for hypertension.
Discussion
We present a case with hyponatremia likely due to SIADH and hypokalemia in a patient with SD and systemic autoimmune rheumatic disease. While several cases reported that SD can cause SIADH and subsequently hyponatremia, there is uncertainty regarding hypokalemia. It could be implicated in SD with a potential mechanism causing potassium loss in the renal tubules, but this has yet to be investigated. Patient will continue to be investigated and treated for hyponatremia and hypokalemia. This case serves as a reminder to be aware of hyponatremia having a rare association with SD.