Antidiuretic hormone (ADH) is formed by the hypothalamus but is stored in the neurohypophysis (posterior pituitary gland). ADH is released in response to increased serum osmolality or decreased blood volume. Although as little as a 1 percent change in serum osmolality will stimulate ADH secretion, blood volume must decrease by approximately 10 percent for ADH secretion to be induced. Psychogenic stimuli (e.g., stress, pain, anxiety) also may stimulate ADH release, but the mechanism by which this occurs is unclear.

ADH acts on the epithelial cells of the distal convoluted tubules and the collecting ducts of the kidneys, making them permeable to water. Thus, with ADH, more water is absorbed from the glomerular filtrate into the bloodstream. Without ADH, water remains in the filtrate and is excreted, producing very dilute urine. In contrast, maximal ADH secretion produces very concentrated urine. ADH also is believed to stimulate mild contractions in the pregnant uterus and to aid in promoting milk ejection in lactation, functions similar to those of oxytocin, which also is secreted by the hypothalamus and released by the neurohypophysis.

• Alcohol, phenytoin drugs, -adrenergic drugs, and morphine antagonists may lead to decreased ADH secretion.
• Acetaminophen, barbiturates, cholinergic agents, clofibrate, estrogens, nicotine, oral hypoglycemic agents, cytotoxic agents (e.g., vincristine), tricyclic antidepressants, oxytocin, carbamazepine (Tegretol), and thiazide diuretics may lead to increased ADH secretion.⁴⁵
• Pain, stress, and anxiety may lead to increased ADH secretion.
• Failure to follow dietary and exercise restrictions before the test may alter results.

• Polyuria or altered serum osmolality of unknown etiology, or both, to identify possible alterations in ADH secretion as the cause
• Central nervous system trauma, surgery, or disease that may lead to impaired secretion of ADH
• Differentiation of neurogenic (central) diabetes insipidus from nephrogenic diabetes insipidus:
  • Neurogenic diabetes insipidus is characterized by decreased ADH levels.
  • ADH levels may be elevated in nephrogenic diabetes insipidus if normal feedback mechanisms are intact.
• Known or suspected malignancy associated with syndrome of inappropriate ADH (SIADH) secretion (e.g., oat cell lung cancer, thymoma, lymphoma, leukemia, and carcinoma of the pancreas, prostate gland, and intestine), with the disorder indicated by elevated ADH levels
• Known or suspected pulmonary conditions associated with SIADH secretion (e.g., tuberculosis, pneumonia, and positive pressure mechanical ventilation), with the disorder indicated by elevated ADH levels

Nursing Care Before the Procedure

Client preparation is essentially the same as that for any study involving collection of a peripheral blood sample (see Appendix I).

• The client should fast from food and avoid strenuous exercise for 12 hours before the sample is obtained. It is recommended that drugs that may alter ADH levels be withheld for 12 to 24 hours before the study, although this practice should be confirmed with the person ordering the test.

A venipuncture is performed and the sample collected in a plastic red-topped tube. Plastic is used because contact with glass causes degradation of ADH. The sample should be handled gently to avoid hemolysis and sent to the laboratory immediately.

Nursing Care After the Procedure

Care and assessment after the procedure are the same as for any study involving collection of a peripheral blood sample.

• Resume food and any medications withheld before the test, as well as usual activities.
• Abnormal levels: Note and report increased levels in relation to renin level. Assess for fluid volume excess resulting from sodium and water retention. Monitor I&O, weight gain, edema, and increases in blood pressure. Instruct in diuretic therapy regimen. Note and report decreased levels in relation to sodium level. Assess for fluid volume deficit. Monitor I&O and weight loss. Instruct in long-term fluid, sodium, and corticosteroid therapy regimen.