SIADH and diabetes insipidus (DI) represent opposite poles of antidiuretic hormone (ADH/vasopressin) dysfunction. ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus, stored in the posterior pituitary, and released in response to increased serum osmolality (detected by hypothalamic osmoreceptors) or decreased blood volume/pressure (detected by baroreceptors). ADH acts on V2 receptors in the renal collecting duct, stimulating aquaporin-2 water channel insertion into the luminal membrane, allowing free water reabsorption from the tubular fluid back into the blood. SIADH (Syndrome of Inappropriate ADH): Excessive ADH secretion despite LOW serum osmolality (which should normally suppress ADH). The excess ADH causes inappropriate water reabsorption, diluting the blood and producing DILUTIONAL HYPONATREMIA. Key lab pattern: LOW serum sodium (<135 mmol/L), LOW serum osmolality (<275 mmol/kg), HIGH urine osmolality (>100 mOsm/kg -- urine is inappropriately concentrated), HIGH urine sodium (>40 mEq/L), and the patient appears EUVOLEMIC (no edema, no dehydration). Common causes: CNS disorders (stroke, head trauma, meningitis, encephalitis), pulmonary disease (pneumonia, TB, SCLC -- ectopic ADH production), medications (SSRIs, carbamazepine, cyclophosphamide, vincristine, oxytocin), and postoperative state. Diabetes Insipidus (DI): Insufficient ADH...