Neurology / Renal

SIADH vs Cerebral Salt Wasting vs Diabetes Insipidus

Two hyponatremia mechanisms — and one opposite disorder

SIADH vs Cerebral Salt Wasting vs Diabetes Insipidus
Feature	SIADH	CSW	Diabetes insipidus
Assessment
Serum sodium	LOW (hypotonic hyponatremia)	LOW (hypotonic hyponatremia)	HIGH (hypernatremia) — the OPPOSITE problem
Serum osmolality	Low	Low	High
Urine osmolality	Inappropriately concentrated (>100 mOsm/kg)	Inappropriately concentrated	Inappropriately dilute despite hypernatremia
Urine sodium	Often >30 mEq/L (euvolemic pattern)	Markedly high with volume depletion	Variable; follows water diuresis
Volume status	Euvolemic (clinically)	Hypovolemic	Hypovolemic if losses unreplaced
Urine output	Normal/subnormal	High (salt-rich diuresis)	Very high, dilute polyuria
Mechanism
Mechanism	ADH secreted despite low osmolality (malignancy, drugs, CNS/pulmonary disease, post-op)	Renal salt wasting — classically after SAH; natriuresis drives ADH secondarily	Central: ADH deficiency. Nephrogenic: ADH resistance (lithium, hypercalcemia)
Management
Treatment principle	Restrict free water; consider NaCl/urea; short-course vasopressin antagonists per protocol; correct Na slowly	REPLACE salt AND volume (isotonic ± hypertonic) — restriction worsens it	Replace water (enterally/IV D5); central → desmopressin; nephrogenic → treat cause, Na restriction ± thiazide/amiloride

Comparing: SIADH

LOW (hypotonic hyponatremia)

Low

Inappropriately concentrated (>100 mOsm/kg)

Often >30 mEq/L (euvolemic pattern)

Euvolemic (clinically)

Normal/subnormal

ADH secreted despite low osmolality (malignancy, drugs, CNS/pulmonary disease, post-op)

Restrict free water; consider NaCl/urea; short-course vasopressin antagonists per protocol; correct Na slowly

For healthcare-professional education. Clinical decisions require patient-specific assessment and local protocols.