Antidiuretic Hormone (ADH) Profile
| Antidiuretic Hormone (ADH) Profile | | | |
| Number | | 046557 |
| CPT | | 83930; 84588 |
| Synonyms | | ADH ; Arginine Vasopressin ; AVP ; Vasopressin |
| Test Includes | | ADH; osmolality |
| Specimen | | Serum and plasma, frozen |
| Volume | | 1 mL serum and 2 mL plasma |
| Minimum Volume | | 0.5 mL serum and 1 mL plasma (Note: This volume does not allow for repeat testing.) |
| Container | | Gel-barrier tube and lavender-top (EDTA) tube |
| Collection | | Draw serum and plasma samples and separate from cells using a refrigerated centrifuge. Transfer separated samples into clearly labeled “plasma” and “serum” plastic transport tubes. Freeze plasma immediately and refrigerate serum. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested. |
| Storage Instructions | | Freeze plasma immediately. Refrigerate serum. |
| Patient Preparation | | No isotopes administered 24 hours prior to venipuncture |
| Causes for Rejection | | Recently administered isotopes; serum specimen not received; plasma specimen not received frozen |
| Reference Interval | | ADH: 0.0-4.7 pg/mL Osmolality: - Neonates: may be as low as 266 mOsmol/kg
- 0-60 years: 275-295 mOsmol/kg
- >60 years: 280-301 mOsmol/kg
|
| Use | | Aid in the diagnosis of urine concentration disorders, especially diabetes insipidus, syndrome of inappropriate ADH (SIADH), psychogenic water intoxication, and syndromes of ectopic ADH production |
| Limitations | | This procedure may be considered by Medicare and other carriers as investigational and, therefore, may not be payable as a covered benefit for patients. |
| Methodology | | ADH: radioimmunoassay (RIA); osmolality: freezing point depression |
| Additional Information | | ADH, produced in the supraoptic and paraventricular locations of the hypothalamus, acts on the collecting tubules of the kidney to cause increase in permeability to water and urea. ADH release is triggered by a number of both osmotic and nonosmotic stimuli. Measurement of ADH is useful in separating central diabetes insipidus, which is marked by polydipsia and polyuria and is caused by inadequate ADH production from nephrogenic diabetes insipidus caused by the inability of renal tubules to respond to ADH. In SIADH, release of ADH is disproportionate to a low serum osmolality. SIADH results due to a number of conditions such as pulmonary disease, head trauma, and cancer. |
| References | | Cowley AW Jr, Cushman WC, Quillen EW Jr, et al, “Vasopressin Elevation in Essential Hypertension and Increased Responsiveness to Sodium Intake,” Hypertension, 1981, 3(3 Pt 2):I93-100. Malvin RL, “Possible Role of the Renin-Angiotensin System in the Regulation of Antidiuretic Hormone Secretion,” Fed Proc, 1971, 30(4):1383-6. Pullan PT, Clappison BH, and Johnston CI, “Plasma Vasopressin and Human Neurophysins and Physiological and Pathological States Associated With Changes in Vasopressin Secretion,” J Clin Endocrinol Metab, 1979, 49(4):580-7. |
|