Medication Summary
The medications described below are used in patients with diabetes insipidus who have hypernatremia.
Vasopressin and vasopressin analogs
Class Summary
Desmopressin is a synthetic ADH with actions mimicking vasopressin. These agents are used to treat diabetes insipidus, which deprives the kidney of its capacity to produce concentrated urine. This effect results in large volumes of dilute urine (polyuria) and excessive thirst (polydipsia). Serum sodium concentrations may be elevated, but hypernatremia is most likely to be severe when fluid is restricted.
Desmopressin acetate (DDAVP)
Structural analog of vasopressin (ADH), the endogenous posterior pituitary hormone that maintains serum osmolality in a physiologically acceptable range. Works in neurohypophysial (eg, central) diabetes insipidus. Exerts similar antidiuretic effects. Vasopressin increases resorption of water at level of renal collecting duct, reducing urinary flow and increasing urine osmolality.
Vasopressin (Pitressin)
Exogenous, parenteral form of ADH. Antidiuretic and increases resorption of water at renal collecting ducts.
Diuretics
Class Summary
These drugs promote the excretion of water and electrolytes by the kidneys. They are used in patients with nephrogenic diabetes insipidus.
Hydrochlorothiazide (Esidrix, HydroDIURIL)
Works by increasing excretion of sodium, chloride, and water by inhibiting sodium ion transport across renal tubular epithelium. Resulting sodium depletion reduces glomerular filtration rate, enhancing reabsorption of fluid in proximal portion of nephron, decreasing delivery of sodium to ascending limb of loop of Henle and consequently reducing capacity to dilute urine.
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Pediatric Hypernatremia. 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.
