Hyponatremic disorders due to vasopressin excess.
Vasopressin is capable of being stimulated by several nonosmotic factors such as hypovolemia, hypotension, pharmacologic agents and stress. Vasopressin levels of only 1-2 pg/ml are capable of decreasing substantially renal water excretion. If water is ingested or given intravenously in this setting, positive water balance with hypotonicity and hyponatremia of extracellular fluid (ECF) occur. Such dilution of the ECF results in water movement into cells and potential central nervous system complications [3]. Many disorders (see Tab. 1) may be associated with nonosmotic stimulation of vasopressin release. In these clinical settings, judicious administration of free water and monitoring of serum sodium concentration is necessary. A knowledge of clinical conditions associated with vasopressin-mediated water retention may have therapeutic implications as well. Thus, in recent years it has become appreciated that selected pharmacologic agents such as lithium and demeclocycline can impair the water retaining property of vasopressin [26]. Although lithium appears too toxic for routine usage, demeclocycline has proved to be efficacious therapy in some patients with high vasopressin levels and hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone who are unable to limit their water intake [9]. More recently, other compounds that selectively antagonize the hydro-osmotic effect of vasopressin are being tested and soon may be available [13].