Antidiuretic Hormone (ADH), Plasma

Plasma, frozen

2 mL

Lavender-top (EDTA) tube

No isotopes administered within 24 hours prior to venipuncture.

Useful for the differential diagnosis of patients with water balance disorders, including diabetes insipidus in conjunction with osmolality and hydration status

This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

The assessment of circulating ADH levels is challenging because it is released in a pulsatile pattern and is rapidly cleared from plasma. Measurement of ADH is further complicated by the high ex vivo instability of the peptide.^1-3

Mixed forms of diabetes insipidus (DI) can exist, and both central and peripheral DI may be incomplete, complicating the interpretation of results.

Radioimmunoassay (RIA)

Antidiuretic Hormone (ADH), also known as Arginine Vasopressin (AVP), is a neuropeptide that is secreted from the hypothalamus in response to hypovolemia and elevated plasma osmolality.^4-6 ADH has two primary functions: to retain water in the body and to constrict blood vessels.⁵ The measurement of ADH has been employed in the differential diagnosis of a variety of disorders related to the physiologic response to changes in plasma osmolality and non-osmotic stress.^1,7 ADH measurement can aid in the differential diagnosis of conditions including diabetes insipidus (DI) and primary polydipsia.

Diabetes insipidus (DI) is a rare disorder of water homeostasis characterized by the excretion of abnormally large volumes of hypotonic urine due to the inability to appropriately concentrate urine in response to volume and osmolar stimuli.^8,9 The primary causes for DI are decreased ADH production (central DI) or decreased renal response to ADH (nephrogenic DI), both of which lead to hypotonic polyuria which is usually accompanied by polydipsia. Along with these etiologies, the differential diagnosis of hypotonic polyuria includes primary polydipsia.^9-11 In primary polydipsia, there is no initial compromise in ADH secretion or renal action and instead, excessive fluid intake leads to a drop in plasma osmolality and a suppression of ADH synthesis. Primary polydipsia can be caused by an abnormality in the thirst center (dipsogenic polydipsia) or, more commonly, as the result of one of a number of psychiatric disorders (psychogenic polydipsia).⁹

Historically, the primary diagnostic test for the evaluation of polyuria-polydipsia syndrome has been the standard water deprivation test.^12-14 In healthy subjects, water deprivation causes the plasma osmolality to rise, leading to the release of ADH into the circulation. In this test, insufficient ADH secretion or effect is revealed by insufficient concentration capacity of the kidneys on osmotic stimulation, which is achieved by a prolonged period of thirsting and followed by assessment of the response to exogenous ADH administration (Desmopressin). Recent studies aimed at validating the classical water deprivation revealed a diagnostic accuracy of only around 70%, with an even lower diagnostic accuracy in patients with primary polydipsia.^3,12 Direct measurement of ADH upon osmotic stimulation has been proposed as an alternative to measuring 24-hour urine osmolality.¹⁵