Does SIADH Cause Frequent Urination?
No, SIADH does not cause frequent urination (polyuria); in fact, it typically results in concentrated urine with reduced urine output due to inappropriate water retention. 1
Pathophysiology of Urination in SIADH
SIADH is characterized by persistent or elevated plasma arginine vasopressin (AVP) despite hyponatremia and low plasma osmolality, leading to water retention rather than increased urination. 1 The concentrated urine with high sodium content results from this inappropriate ADH activity, where fluid balance is maintained at the expense of plasma sodium through a physiologic natriuresis. 1
Key Urinary Characteristics in SIADH
- Urine osmolality is inappropriately high (>500 mosm/kg) despite low serum osmolality, indicating the kidneys are retaining water rather than excreting it 1, 2
- Urinary sodium concentration is elevated (>20-40 mEq/L) due to compensatory natriuresis, not increased urine volume 1, 2
- Urine volume is typically normal or reduced, not increased, as the hallmark of SIADH is water retention 3
Clinical Presentation
The cardinal diagnostic criteria for SIADH include 1, 2:
- Hyponatremia (serum sodium <134 mEq/L)
- Hypoosmolality (plasma osmolality <275 mosm/kg)
- Inappropriately concentrated urine (>500 mosm/kg) - this means less urine output, not more
- Elevated urinary sodium (>20 mEq/L)
- Euvolemia (absence of volume depletion or overload)
- Normal renal, adrenal, and thyroid function
Symptoms of SIADH relate to hyponatremia severity, not urinary frequency. 4 When hyponatremia is severe (≤125 mEq/L), patients may experience anorexia, vomiting, confusion, seizures, or coma. 4, 5 Neuromuscular and gastrointestinal symptoms predominate, with severity related to both the absolute serum sodium concentration and its rate of fall. 3
Common Pitfall
A critical diagnostic error is confusing SIADH with conditions that do cause polyuria, such as diabetes insipidus or cerebral salt wasting (CSW). 1, 6 In neurosurgical patients particularly, distinguishing SIADH from CSW is essential, as CSW presents with true hypovolemia and may have higher urine output, requiring opposite treatment (volume replacement rather than fluid restriction). 1, 6
Treatment Implications
The mainstay of SIADH treatment is fluid restriction to 1 L/day, which would be counterproductive if the patient were experiencing polyuria. 1, 4, 5 For chronic SIADH, fluid restriction remains the cornerstone therapy, with demeclocycline or vasopressin receptor antagonists reserved for refractory cases. 1, 4, 7