Posters
Presenting Author Academic/Professional Position
Raquel Z Lara
Academic Level (Author 1)
Medical Student
Academic Level (Author 2)
Resident
Discipline/Specialty (Author 2)
Internal Medicine
Academic Level (Author 3)
Resident
Discipline/Specialty (Author 3)
Internal Medicine
Academic Level (Author 4)
Resident
Discipline/Specialty (Author 4)
Internal Medicine
Discipline Track
Clinical Science
Abstract Type
Case Report
Abstract
Background: Hyponatremia is an electrolyte disturbance with various etiologies, but hypothyroidism is rarely the primary cause. Literature suggests that hypothyroidism-related hyponatremia occurs primarily in severe cases, with some studies suggesting that hypothyroidism should not be considered a sole contributor if TSH levels are below 50 mIU/L. Patients with hyponatremia have a high risk of prolonged hospital stays and readmission, underscoring the clinical importance of identifying uncommon causes such as severe hypothyroidism. This case highlights this rare association, contributing to the existing limited literature.
Case Presentation: A 74-year-old woman with Type 2 Diabetes, complicated nephrotic syndrome and nephropathy, congestive heart failure, and hypertension, presented with generalized weakness, progressive extremity swelling, and orthopnea persisting for several weeks. Lab work on admission showed a TSH of 139, a T4 of 0.27, a sodium level of 130, and a serum osmolality of 281. Urinalysis revealed a creatinine of 41, osmolality of 347, protein over 200, and sodium of 60, indicative of hypotonic hypervolemic hyponatremia. Cortisol levels were within normal limits, and echocardiogram showed a left ventricular ejection fraction of 60%.
Initial management following Endocrinology recommendations consisted of fluid restriction to 1 L per day and diuresis with IV Lasix, which was discontinued after four days. The patient was started on IV levothyroxine to which she partially responded to, but TSH levels increased to 191.68, worsening her hyponatremia to 128. Treatment was adjusted to include sodium chloride supplementation (2 g twice daily) and oral liothyronine for severe hypothyroidism. The patient’s condition gradually improved, with resolution of symptoms and stabilization of her sodium levels after 18 days.
Conclusions: This case illustrates severe hypothyroidism as the primary contributor for the development of this patient’s refractory hyponatremia, despite correcting other potential etiologies such as nephrotic syndrome and congestive heart failure. The resolution of the patient's symptoms and the improvement in sodium levels following thyroid hormone administration further suggests that profound hypothyroidism can significantly influence sodium homeostasis. Clinicians should consider severe hypothyroidism as a potential cause of unexplained or refractory hyponatremia in patients with multiple comorbidities to ensure timely diagnosis and optimal management.
Presentation Type
Poster
Recommended Citation
Lara, Raquel Z.; Swamy, Tejaswini; Rojas Huen, Jennifer; and Serna, Ricardo, "The Sodium Chronicles: Unraveling the Enigma of Hypothyroidism-Induced Hyponatremia" (2025). Research Colloquium. 85.
https://scholarworks.utrgv.edu/colloquium/2025/posters/85
The Sodium Chronicles: Unraveling the Enigma of Hypothyroidism-Induced Hyponatremia
Background: Hyponatremia is an electrolyte disturbance with various etiologies, but hypothyroidism is rarely the primary cause. Literature suggests that hypothyroidism-related hyponatremia occurs primarily in severe cases, with some studies suggesting that hypothyroidism should not be considered a sole contributor if TSH levels are below 50 mIU/L. Patients with hyponatremia have a high risk of prolonged hospital stays and readmission, underscoring the clinical importance of identifying uncommon causes such as severe hypothyroidism. This case highlights this rare association, contributing to the existing limited literature.
Case Presentation: A 74-year-old woman with Type 2 Diabetes, complicated nephrotic syndrome and nephropathy, congestive heart failure, and hypertension, presented with generalized weakness, progressive extremity swelling, and orthopnea persisting for several weeks. Lab work on admission showed a TSH of 139, a T4 of 0.27, a sodium level of 130, and a serum osmolality of 281. Urinalysis revealed a creatinine of 41, osmolality of 347, protein over 200, and sodium of 60, indicative of hypotonic hypervolemic hyponatremia. Cortisol levels were within normal limits, and echocardiogram showed a left ventricular ejection fraction of 60%.
Initial management following Endocrinology recommendations consisted of fluid restriction to 1 L per day and diuresis with IV Lasix, which was discontinued after four days. The patient was started on IV levothyroxine to which she partially responded to, but TSH levels increased to 191.68, worsening her hyponatremia to 128. Treatment was adjusted to include sodium chloride supplementation (2 g twice daily) and oral liothyronine for severe hypothyroidism. The patient’s condition gradually improved, with resolution of symptoms and stabilization of her sodium levels after 18 days.
Conclusions: This case illustrates severe hypothyroidism as the primary contributor for the development of this patient’s refractory hyponatremia, despite correcting other potential etiologies such as nephrotic syndrome and congestive heart failure. The resolution of the patient's symptoms and the improvement in sodium levels following thyroid hormone administration further suggests that profound hypothyroidism can significantly influence sodium homeostasis. Clinicians should consider severe hypothyroidism as a potential cause of unexplained or refractory hyponatremia in patients with multiple comorbidities to ensure timely diagnosis and optimal management.
