Abstract: PUB155
Severe Hyponatremia Secondary to Hypothyroidism: A Reversible Cause
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Zaw, Thet N., Coffee Regional Medical Center, Douglas, Georgia, United States
- Carter, Ashlyn, Coffee Regional Medical Center, Douglas, Georgia, United States
Introduction
Hyponatremia is a common and potentially serious electrolyte disturbance in elderly patients. While syndrome of inappropriate antidiuretic hormone secretion (SIADH) and volume-related causes are frequently considered, severe hypothyroidism is an underrecognized but reversible etiology that can impair free water excretion.
Case Description
A 93-year-old female presented with altered mental status and generalized weakness. Initial labs revealed severe hyponatremia (Na 120 mmol/L) and a markedly elevated thyroid-stimulating hormone (TSH) of 123.34 µIU/mL. She appeared euvolemic on physical exam. Urine studies showed specific gravity 1.010, urine sodium 63 mmol/L, urine potassium 40 mmol/L, and urine chloride 57 mmol/L, consistent with impaired water excretion in the absence of diuretics or hypovolemia. Adrenal function was normal. The clinical and laboratory picture suggested hypothyroidism-induced hyponatremia.
Levothyroxine therapy was initiated. Over the next month, TSH levels progressively declined (to 27.84 µIU/mL by September 29), and serum sodium improved to 133 mmol/L. The patient’s cognitive function and energy level improved in parallel with biochemical recovery. No fluid restriction or hypertonic saline was required, supporting thyroid hormone deficiency as the primary driver of her hyponatremia.
Discussion
Hyponatremia is often multifactorial in elderly patients, and hypothyroidism may not be routinely considered in the initial workup. However, thyroid hormone deficiency can significantly impact renal water handling, cardiac output, and vasopressin regulation. In this case, she exhibited a euvolemic profile with inappropriate urinary sodium and impaired urine dilution, suggesting SIADH-like physiology, but without a clear trigger other than profound hypothyroidism. The improvement of sodium levels following thyroid hormone replacement, without other interventions, confirms the endocrine cause.
The mechanisms by which hypothyroidism leads to hyponatremia include:
1) Reduced cardiac output → perceived hypovolemia → non-osmotic ADH release
2) Decreased GFR and impaired renal water clearance
3) Reduced Na/K ATPase activity → impaired tubular sodium reabsorption
This case underlines the importance of evaluating thyroid function in all cases of unexplained or persistent hyponatremia. Recognition and correction with levothyroxine can safely reverse the sodium imbalance without additional interventions.