Cerebral salt wasting (CSW) is an uncommon but clinically significant syndrome of renal sodium loss and volume depletion that occurs in the setting of central nervous system (CNS) disease, most commonly following subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), neurosurgery, and CNS tumors. The hallmark of CSW is hyponatremia caused by primary renal sodium wasting, resulting in true extracellular volume depletion -- a critical distinction from the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which produces dilutional hyponatremia in a euvolemic or mildly hypervolemic state. The pathogenesis of CSW remains incompletely understood but involves two primary mechanisms that drive inappropriate natriuresis despite volume depletion. The first mechanism involves the release of natriuretic peptides from damaged brain tissue, particularly brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP). Following CNS injury, damaged neurons and glial cells release BNP into the circulation. BNP binds to natriuretic peptide receptor A (NPR-A) on renal tubular cells, activating guanylyl cyclase and increasing intracellular cyclic guanosine monophosphate (cGMP), which directly inhibits sodium reabsorption in the collecting duct and suppresses renin secretion from the juxtaglomerular apparatus. The...