Medication Summary
Maintenance of adequate fluid intake is the most important therapy for all causes of DI that can result in hypernatremia. Hormonal and pharmacologic therapies must be tailored for the specific causes of DI (eg, central, nephrogenic). Central DI is treated with replacement therapy of ADH. The therapy for nephrogenic DI depends on reducing urine volume with combinations of salt restriction, thiazide diuretics, and prostaglandin synthetase inhibitors.
The other causes of hyponatremia do not require medications beyond hypotonic fluid for correction.
ADH replacement therapy
Class Summary
This therapy reduces free water loss and concentrates the urine.
Vasopressin (Pitressin)
Has vasopressor and ADH activity. Increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). Vasoconstriction also is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels. Decreases portal pressure in patients with portal hypertension. A notable undesirable effect is coronary artery constriction, which may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates. Duration of action is approximately 3-6 h. Short half-life lessens the risk of acute water intoxication and makes it the ideal treatment of central DI in emergent situations.
Desmopressin acetate (DDAVP)
Increases cellular permeability of collecting ducts, resulting in reabsorption of water by the kidneys. Duration of action is approximately 12-24 h. Has become the long-term treatment of choice for central DI.
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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
