The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an endocrine disease, characterized by inappropriately concentrated urine, dilutional hyponatremia, and subsequent manifestations of various central nervous system (CNS) symptoms. Though usually transient, SIADH may be chronic. It is often associated with drug use or a lesion in the central nervous system or lung. SIADH is divided into two categories. One is the ectopic ADH syndrome induced by abnormally secreted arginine vasopressin (ADH/AVP) from cancer cells. Another is the morbidity caused by inappropriately secreted ADH from the pituitary gland. In both situations of SIADH, ADH binds to vasopressin V2 receptors (V2Rs) in renal tubules and thereby increasing water reabsorption. SIADH is difficult to distinguish from cerebral salt wasting syndrome (CSWS), another cause of hyponatremia characterized by renal loss of sodium and decreases in extracellular fluid volume during intracranial disorders. SIADH occurs in the setting of euvolemia, without evidence of renal disease or thyroxine or cortisol deficiency. Treatment options for SIADH include fluid restriction, demeclocycline, urea, frusemide and saline infusion, all of which have their limitations. The introduction of the vasopressin-2 receptor antagonists has allowed clinicians to specifically target the underlying pathophysiology of SIADH.
Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is characterized by a clinical picture similar to SIADH, but is associated with undetectable levels of AVP.
