Clinical meaning
SIADH results from excessive secretion of antidiuretic hormone (ADH/vasopressin) from the posterior pituitary or ectopic sources, independent of normal osmotic or volume stimuli. ADH acts on V2 receptors in the renal collecting ducts, inserting aquaporin-2 channels that dramatically increase water reabsorption from the tubular filtrate back into the bloodstream. This pathological water retention leads to expansion of extracellular fluid volume, dilutional hyponatremia (serum Na often <130 mEq/L), decreased serum osmolality (<275 mOsm/kg), and paradoxically concentrated urine (osmolality >100 mOsm/kg) with elevated urine sodium (>40 mEq/L). The brain is particularly vulnerable: as serum sodium falls, water moves into brain cells via osmosis, causing cerebral edema. Mild hyponatremia (Na 125-134) causes headache, nausea, and confusion. Severe hyponatremia (Na <120) can trigger seizures, coma, brainstem herniation, and death. Importantly, the patient appears euvolemic - no peripheral edema, no signs of dehydration - because the excess water distributes across total body water rather than accumulating in a visible compartment. This euvolemic state with hypo-osmolality is the hallmark that distinguishes SIADH from other causes of hyponatremia.