Syndrome of Inappropriate Antidiuretic Hormone Secretion
A 22-year-old woman is admitted after two generalised tonic-clonic seizures. MRI shows a ring-enhancing right temporal mass, and biopsy confirms glioblastoma multiforme. There is no postural blood pressure drop and no peripheral oedema. Serum sodium is 118 mmol/L, serum osmolality 250 mosmol/kg, urine osmolality 620 mosmol/kg, urine sodium 65 mmol/L, and serum uric acid 130 µmol/L. Which of the following is the most likely cause of her hyponatraemia?
- A.Renal salt-wasting nephropathy
- B.Excessive free water consumption
- C.High intake of sugar-sweetened drinks
- D.Inappropriate antidiuretic hormone secretionCorrect
Explanation
This patient has hypotonic hyponatraemia with clinical euvolaemia, inappropriately concentrated urine (osmolality 620 mosmol/kg when it should be maximally dilute at under 100), a urine sodium above 40 mmol/L, and a low serum uric acid, with normal thyroid and adrenal function. That constellation defines the syndrome of inappropriate antidiuretic hormone secretion. Central nervous system disorders, including intracranial tumours, seizures, meningitis, and head injury, are a classic trigger, and antiepileptic drugs such as carbamazepine can contribute. Persistent antidiuretic hormone action causes water retention with secondary natriuresis, which keeps the patient euvolaemic rather than oedematous and explains the high urine sodium and the low uric acid from increased fractional urate excretion. Cerebral or renal salt wasting is the main mimic but produces genuine volume depletion with orthostatic hypotension, weight loss, and a high urine output, none of which are present here. Primary polydipsia can lower sodium but overwhelms the diluting mechanism only when water intake is enormous, and the urine would then be maximally dilute with osmolality below 100 mosmol/kg. Sugar-sweetened drinks do not cause chronic hypotonic hyponatraemia, and a high glucose load would produce translocational hyponatraemia with normal or raised serum osmolality. Treatment is fluid restriction with treatment of the underlying cause; severe symptomatic hyponatraemia with seizures requires hypertonic 3 percent saline, with correction limited to 8 mmol/L in 24 hours to avoid osmotic demyelination.
Why each option
- A.
- Salt wasting causes true hypovolaemia with orthostatic hypotension, weight loss, and high urine volumes, none of which this euvolaemic patient shows.
- B.
- Primary polydipsia produces maximally dilute urine with an osmolality below 100 mosmol/kg, not the concentrated urine seen here.
- C.
- Sugar-sweetened drinks do not cause chronic hypotonic hyponatraemia; a glucose load causes translocational hyponatraemia with a normal serum osmolality.
- D.
- Correct. Euvolaemic hypotonic hyponatraemia with concentrated urine, urine sodium above 40 mmol/L, and low uric acid in a patient with a brain tumour is SIADH.
Reference: European Clinical Practice Guideline on Diagnosis and Treatment of Hyponatraemia, 2014; UpToDate 2025, Pathophysiology and etiology of SIADH
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