Antidiuretic Hormone (ADH), Plasma

CPT: 84588
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  • Arginine Vasopressin, AVP
  • Vasopressin

Expected Turnaround Time

4 - 12 days

Related Information

Related Documents

Specimen Requirements


Plasma, frozen


2 mL


Lavender-top (EDTA) tube


Centrifuge in a refrigerated centrifuge, separate plasma, and freeze immediately. Transfer specimen to a plastic transport tube before freezing. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

Storage Instructions


Patient Preparation

No isotopes administered within 24 hours prior to venipuncture.

Causes for Rejection

Recently administered isotopes; plasma specimen not received frozen

Test Details


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)

Additional Information

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


1. Christ-Crain M. Diabetes insipidus - new concepts for diagnosis. Neuroendocrinology. 2020;110(9-10):859-867.31986514
2. Refardt J. Diagnosis and differential diagnosis of diabetes insipidus: Update. Best Pract Res Clin Endocrinol Metab. 2020 Sep;34(5):101398.32387127
3. Fenske WK, Schnyder I, Koch G, et al. Release and Decay Kinetics of Copeptin vs AVP in Response to Osmotic Alterations in Healthy Volunteers. J Clin Endocrinol Metab. 2018 Feb 1;103(2):505-513.29267966
4. Bichet DG. Vasopressin and the Regulation of Thirst. Ann Nutr Metab. 2018;72 Suppl 2:3-7.29925072
5. Bankir L, Bichet DG, Morgenthaler NG. Vasopressin: physiology, assessment and osmosensation. J Intern Med. 2017 Oct;282(4):284-297.28649750
6. Balanescu S, Kopp P, Gaskill MB, Morgenthaler NG, Schindler C, Rutishauser J. Correlation of plasma copeptin and vasopressin concentrations in hypo-, iso-, and hyperosmolar States. J Clin Endocrinol Metab. 2011 Apr;96(4):1046-1052.21289257
7. Rosen CJ, Ingelfinger JR. A Reliable Diagnostic Test for Hypotonic Polyuria. N Engl J Med. 2018 Aug 2;379(5):483-484.30067935
8. Garrahy A, Moran C, Thompson CJ. Diagnosis and management of central diabetes insipidus in adults. Clin Endocrinol (Oxf). 2019 Jan;90(1):23-30.30269342
9. Christ-Crain M, Fenske W. Copeptin in the diagnosis of vasopressin-dependent disorders of fluid homeostasis. Nat Rev Endocrinol. 2016 Mar;12(3):168-176.26794439
10. Verbalis JG. Acquired forms of central diabetes insipidus: Mechanisms of disease. Best Pract Res Clin Endocrinol Metab. 2020 Sep;34(5):101449.32792133
11. Ahmadi L, Goldman MB. Primary polydipsia: Update. Best Pract Res Clin Endocrinol Metab. 2020 Sep;34(5):101469.33222764
12. Fenske W, Quinkler M, Lorenz D, et al. Copeptin in the differential diagnosis of the polydipsia-polyuria syndrome--revisiting the direct and indirect water deprivation tests. J Clin Endocrinol Metab. 2011 May;96(5):1506-1515.21367924
13. Fenske W, Refardt J, Chifu I, et al. A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus. N Engl J Med. 2018 Aug 2;379(5):428-439.30067922
14. Timper K, Fenske W, Kühn F, et al. Diagnostic Accuracy of Copeptin in the Differential Diagnosis of the Polyuria-polydipsia Syndrome: A Prospective Multicenter Study. J Clin Endocrinol Metab. 2015 Jun;100(6):2268-2274.25768671
15. Zerbe RL, Robertson GL. A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria. N Engl J Med. 1981 Dec 24;305(26):1539-1546.7311993


Cowley AW Jr, Cushman WC, Quillen EW Jr, Skelton MM, Langford HG. Vasopressin elevation in essential hypertension and increased responsiveness to sodium intake. Hypertension. 1981 May-Jun; 3(3 Pt 2):I93-100. 7262983
Malvin RL. Possible role of the renin-angiotensin system in the regulation of antidiuretic hormone secretion. Fed Proc. 1971 Jul-Aug; 30(4):1383-1386. 4326738
Pullan PT, Clappison BH, Johnston CI. Plasma vasopressin and human neurophysins in physiological and pathological states associated with changes in vasopressin secretion. J Clin Endocrinol Metab. 1979 Oct; 49(4):580-587. 479348
Rascher W, Rauh W, Brandeis WE, Huber KH, Schärer K. Determinants of plasma arginine-vasopressin in children.Acta Paediatr Scand. 1986 Jan; 75(1):111-117. 3953266


Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
010447 ADH 3126-0 010449 ADH pg/mL 3126-0

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