DI Vs. SIADH: Fluid and Electrolyte

Antidiuretic hormone (ADH/vasopressin) is synthesized in the hypothalamus and released from the posterior pituitary in response to increased serum osmolality or decreased blood volume. ADH acts on V2 receptors in the renal collecting duct, inserting aquaporin-2 channels to increase water reabsorption. In Diabetes Insipidus (DI), ADH is either insufficient (central DI from pituitary damage) or the kidneys are unresponsive to ADH (nephrogenic DI from lithium, renal disease). This causes massive water loss producing dilute urine (specific gravity <1.005, osmolality <300 mOsm/kg) and hypernatremia from free water deficit. In SIADH, excess ADH causes inappropriate water retention, producing concentrated urine (specific gravity >1.030, osmolality >100 mOsm/kg) and dilutional hyponatremia. SIADH is associated with small cell lung cancer (ectopic ADH), brain injury, certain medications (SSRIs, carbamazepine), and pulmonary disease.