Medication Summary
Treatment for diabetes insipidus (DI) varies with the form of the disorder. In central DI and most cases of gestational DI, the primary problem is a deficiency of antidiuretic hormone (ADH)—also known as arginine vasopressin (AVP)—and therefore, physiologic replacement with desmopressin is usually effective. A nonhormonal drug can be used if response is incomplete or desmopressin is too expensive.
Desmopressin has no role in the treatment of nephrogenic DI or primary polydipsia. Nonhormonal drugs usually are more effective in treating nephrogenic DI.
Vasopressin-Related Hormones
Class Summary
In patients with central DI, replacement of endogenous ADH with exogenous hormones prevents complications of DI and reduces morbidity.
Desmopressin (DDAVP, Stimate)
Desmopressin is a synthetic analogue of ADH with potent antidiuretic activity but no vasopressor activity.
Vasopressin (Pitressin)
Vasopressin has vasopressor and ADH activity. It increases water resorption at collecting ducts (ADH effect). At high doses, it also promotes smooth muscle contraction throughout the vascular bed of renal tubular epithelium (vasopressor effects). However, vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.
Antidiabetics, Sulfonylureas
Class Summary
The hypoglycemic agent chlorpropamide helps to relieve diuresis in patients with DI.
Chlorpropamide
Chlorpropamide promotes renal response to ADH.
Anticonvulsants
Class Summary
Certain antiepileptic drugs, such as carbamazepine, have proven helpful in DI.
Carbamazepine (Tegretol, Carbatrol, Equetro)
Carbamazepine possibly ameliorates DI by promoting the release of ADH. It is not useful in nephrogenic DI and generally is not a first-line drug.
Diuretics, Thiazide
Class Summary
Diuretics may reduce flow to the ADH-sensitive distal nephron.
Hydrochlorothiazide (Microzide)
Hydrochlorothiazide is a thiazide diuretic that decreases urinary volume in the absence of ADH. It may induce mild volume depletion and cause proximal salt and water retention, thereby reducing flow to the ADH-sensitive distal nephron. Its effects are additive to those of other agents.
Nonsteroidal Anti-inflammatory Agents (NSAIDs)
Class Summary
The mechanism of action of NSAIDs is not known, but these agents may act by inhibiting prostaglandin synthesis.
Indomethacin (Indocin)
Inhibition of prostaglandin synthesis reduces the delivery of solute to distal tubules, reducing urine volume and increasing urine osmolality. Indomethacin is usually used in nephrogenic DI.
Ibuprofen (Caldolor, Advil, Motrin)
Inhibition of prostaglandin synthesis reduces the delivery of solute to distal tubules, reducing urine volume and increasing urine osmolality. Ibuprofen is usually used in nephrogenic DI.
Naproxen (Naprosyn, Naprelan, Aleve, Anaprox)
Diclofenac (Voltaren, Cataflam XR, Zipsor, Cambia)
Ketoprofen
Inhibition of prostaglandin synthesis reduces the delivery of solute to distal tubules, reducing urine volume and increasing urine osmolality.
Diuretics, Potassium-Sparing
Class Summary
Diuretics may reduce flow to the ADH-sensitive distal nephron.
Amiloride
Amiloride is a potassium-sparing diuretic. Thus, the risk of hypokalemia is decreased when amiloride is used in combination with hydrochlorothiazide. In addition, the 2 agents are synergistic with respect to antidiuresis.