What is the diagnosis and management for a euvolemic patient with a urine sodium level of 75 and urine osmolality of 571, suggesting impaired renal function?

Diagnosis: Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

This euvolemic patient with urine sodium >40 mEq/L (75 mEq/L) and inappropriately concentrated urine (osmolality 571 mOsm/kg) has SIADH until proven otherwise.

Diagnostic Reasoning

The combination of clinical and laboratory findings points definitively toward SIADH:

• Euvolemic status excludes hypovolemic (prerenal) and hypervolemic causes of concentrated urine 1
• Elevated urine sodium (75 mEq/L) indicates continued renal sodium excretion despite what should trigger sodium conservation, characteristic of SIADH 1
• Inappropriately concentrated urine (571 mOsm/kg) demonstrates the kidney's inability to excrete free water due to excessive ADH activity 1

Key Distinguishing Features

In prerenal azotemia or volume depletion, urine sodium should be <20 mEq/L (often <10 mEq/L), with fractional excretion of sodium (FENa) <1% 1, 2. This patient's urine sodium of 75 mEq/L excludes volume depletion 1.

In acute tubular necrosis (ATN), urine sodium is typically >40 mEq/L, but urine osmolality would be isosthenuric (250-350 mOsm/kg), not concentrated 3, 2. The high urine osmolality (571 mOsm/kg) excludes ATN 4.

Management Approach

Immediate Actions

• Measure serum sodium, serum osmolality, and BUN/creatinine to confirm hyponatremia and hypoosmolality while excluding renal failure 1
• Identify and treat the underlying cause of SIADH (medications, malignancy, CNS disorders, pulmonary disease) 1
• Discontinue any offending medications that may stimulate ADH release or potentiate its effects 1

Fluid Management Strategy

Restrict total fluid intake to <1 L/day as the cornerstone of SIADH management, though this rarely normalizes sodium and primarily prevents further decline 1.

For severe or symptomatic hyponatremia (serum sodium <130 mEq/L):

• Consider vaptans (V2-receptor antagonists) such as tolvaptan, which selectively block ADH action in collecting ducts and improve serum sodium in 45-82% of patients 1
• Avoid hypertonic saline in chronic SIADH as efficacy is partial, short-lived, and may worsen volume status 1
• Monitor for overly rapid correction to prevent osmotic demyelination syndrome; aim for correction <8-10 mEq/L per 24 hours 1

Critical Pitfalls to Avoid

• Do not assume volume depletion based solely on elevated BUN or creatinine without assessing urine indices—this patient's high urine sodium excludes prerenal azotemia 1, 2
• Do not administer isotonic saline thinking this will correct hyponatremia; in SIADH, the kidneys will excrete the sodium and retain the free water, paradoxically worsening hyponatremia 1
• Do not use demeclocycline as first-line therapy due to significant side effects and inconsistent efficacy 1

Monitoring Parameters

• Daily serum sodium measurements during active treatment to ensure appropriate correction rate 1
• Daily weights and clinical volume assessment to confirm euvolemic status is maintained 1, 4
• Urine output and osmolality to assess response to therapy 1