The last time you enjoyed those hot dogs and potato chips and washed them down with beer or soda, you probably didn't wonder how your body was going to get rid of all that extra salt and fluid. You didn't have to wonder because the various receptors in your body, hormonal responses, and your kidneys were ready to take care of that excess for you. All you had to do was find the bathroom.
One of the hormones involved is antidiuretic hormone (ADH). Like all hormones, ADH profoundly affects some life-sustaining functions. Also known as vasopressin, ADH is a 9-amino-acid peptide (see Figure 1) packaged with a carrier protein.  Present in plasma at [less than] 2 pmol/L,  ADH promotes various physiologic functions,  one of which is to maintain water homeostasis, which in turn helps maintain normal volume for plasma and interstitial and intracellular fluids. Major fluctuations in fluid volumes can detrimentally affect plasma electrolyte levels and blood pressure and thus the cardiovascular and central nervous systems. (Because the other fluid compartments cannot be easily sampled in amounts sufficient for chemical analysis, emphasis in this article will be on blood plasma/serum.)
ADH is part of a dynamic balance
Synthesized in the hypothalamus and secreted by the pituitary gland, ADH helps maintain fluid volumes and sodium levels within a vital narrow range. This is accomplished by signaling the renal collecting ducts (see illustration) to actively promote water reabsorption into the systemic circulation.  At first, this may seem confusing, because we often think of water moving passively in the same direction with sodium ions, which is what happens in the presence of the mineralocorticoid, aldosterone, when it promotes active renal tubular reabsorption of sodium (and excretion of potassium).  However, when ADH actively promotes water reabsorption through the renal collecting ducts, the water is reabsorbed at a rate that exceeds the rate of solute reabsorption. Consequently, urinary sodium and chloride concentrations increase while the rate of water collection into the urine decreases. The result is the formation of a more concentrated urine (see Table 1). 
Because the focus of this article is the physiologic and pathologic effects of ADH, by necessity, this subject is viewed in isolation. However, the reader should remember that as water and solutes traverse the kidney, many hormones (such as aldosterone) and other physiologic factors affect the final urine concentration.
Any change in fluid homeostasis affects blood pressure and serum and urine osmolality. Recall that osmolality is a colligative property that depends on the number of moles of all solutes in a kilogram of solvent (usually water) and is expressed as millimols (mmol)/kg or millimoles (mmol)/L. [7,8] Simply stated, the more solute particles present in a fluid, the more concentrated the fluid and the greater its osmotic pressure. Likewise, blood pressure increases as osmolality increases.
The amount of fluid and solutes ingested varies each day and throughout the day, but it is essential for plasma osmolality to remain constant within a reference range of approximately 278-298 mmol/L.  To maintain this plasma steady-state, ADH helps adjust the concentration/osmolality of urine by changing the amount of water reabsorbed through the collecting ducts. Thus, urine osmolalities can range from as low as 50 mmol/L to [greater than] 1,200 mmol/L, depending on the plasma solute load, fluid volume ingested, and other relevant renal factors not discussed here. 
Within the kidney, the molecular sequence responsible for this action begins as ADH binds with its vasopressin-2 receptor (V2R) within cellular membranes in the collecting ducts. This receptor is also linked to stimulatory G-protein. When bound with ADH, V2R (via the G-protein) activates adenylate cyclase, which increases the level of cyclic adenosine monophosphate (CAMP). This important metabolic regulator signals the water-transporting proteins (aquaporin-2) to insert themselves into the cell membranes in the collecting ducts. These cell membranes now allow more water to flow back into the plasma, and consequently, the urine becomes more concentrated. 
At least 2 sets of receptors determine how much ADH is produced by the hypothalamus. Osmoreceptors in the hypothalamus itself cause the pituitary to increase ADH levels when plasma osmolality increases as little as 1-2% [2,7] Baroreceptors, especially in the heart and the carotid sinus,  monitor changes in blood volume and pressure and indirectly signal the hypothalamus to regulate ADH according to perceived changes.
At least one animal study indicates that stretch receptors in the cerebral ventricle wall may also help regulate plasma volume by contributing to the control of ADH levels.  However, this has not yet been confirmed in humans. The thirst center is also located in the hypothalamus and is regulated by many of the same factors that determine ADH release. However, this center has a higher set point than the osmoreceptors and responds to osmolalities[greater than] 290 mmol/L. [1,2]
Like most of our homeostatic mechanisms, the regulatory effects of ADH can be disturbed. When disease, medication, head trauma, or surgical injury upset the feedback system, the result is either diabetes insipidus (DI) or the syndrome of inappropriate antidiuretic hormone (SIADH) (see Table 2).
Diabetes insipidus is essentially the chronic excretion of very large amounts of hypo-osmotic urine in response to the decreased production, secretion, or effect of ADH.  Diabetes insipidus can be categorized as neurogenic and nephrogenic. In neurogenic DI, which is also known as central, cranial,  pituitary,  or hypothalamic  DI, ADH production or secretion is decreased by the hypothalamus or pituitary, respectively. Inadequate formation or release of ADH in neurogenic DI can be partial or complete, depending on the degree of disturbance to the hypothalamus or pituitary gland.  A less common form of central DI is hereditary (autosomal dominant) and manifests during childhood. 
In nephrogenic DI, ADH production and secretion are adequate and appropriate, but the kidneys don't respond to the hormone because of some form of primary renal disease,  medications, or conditions that affect the kidney. This lack of response is typical in association with many types of renal dysfunction because concentrating ability is one of the first functions to be impaired as a result of renal damage.  Nephrogenic DI can also be hereditary and may be present at birth. Consequently, the signs and symptoms must be recognized at that time to avoid severe episodes of dehydration.  Various mutations can produce hereditary nephrogenic DI and are transmitted as sex-linked abnormalities or autosomal recessive or dominant abnormalities. [9,16]
Clinical signs and symptoms. When ADH levels decrease or when the kidneys aren't responding, excess amounts of water are lost into the urine, producing polyuria. This characteristic of DI  is marked by a urinary output greater than normal, which is approximately 2.5 L/day under low-stress conditions.  With complete ADH deficiency, urine output may approach 1 L/hour.  If the thirst center is intact; the patient will be extremely thirsty (polydipsic). When mild to moderate DI is present, conscious patients who are capable of drinking can usually compensate for the water loss by drinking extra fluids. However, if the oral intake can't equal urinary losses, the patient is at risk for dehydration and severe hypernatremia. Appropriate IV fluids are then required, because untreated dehydration causes tachycardia, orthostatic hypotension, poor skin turgor, and dry mucous membranes.  Eventually, untreated dehydration can cause irreversible neurologic damage as the patient spirals downward through lethar gy, confusion, seizures, and even coma.
Diagnosis. There are 3 basic areas of testing to aid in the diagnosis of DI.
Osmolalities and electrolytes. Physiologically, plasma osmolality results provide an indication of total body water osmolality.  Thus, plasma osmolality, along with urine osmolality and serum sodium levels, are the principal laboratory methods used to diagnose ADH abnormalities (see Table 2). The water loss through the kidneys increases both serum osmolality and serum sodium levels to [greater than] 295 mmol/L and [greater than] 145 mmol/L, respectively (normal serum sodium levels are 135--145 mmol/L)  Urine osmolality rarely exceeds 300 mmol/L in either neurogenic or neurologic DI. Patients with partial neurogenic DI may exhibit urine osmolalities between 300 and 800 mmol/L.  In addition to supporting a preliminary diagnosis, these tests are performed if the water deprivation test (discussed later) is ordered.
ADH assays. Although many immunoassays for plasma or urine ADH have been described, none are routinely performed because of their complexity and lack of specificity and sensitivity.  Nonetheless, ADH assays are performed in various reference laboratories, [18-20] and results can support the diagnosis of DI and SIADH.  For most plasma assays, solvents or column chromatography is required as a preliminary extraction and concentration procedure to concentrate the minute amount of ADH in the plasma and to remove interfering substances. Although nonisotopic immunoassays have been developed for ADH, most clinical laboratories use one of several radioimmunoassay procedures [2,19,20] if they perform ADH assays.
Blood specimens for ADH are collected into chilled EDTA tubes, and most procedures require that specimens be delivered to the laboratory on ice and centrifuged at 4[degrees]C within 30 minutes after collection. The plasma is removed and stored at -20[degrees]C until analyzed. Random urine specimens are collected without preservatives, but a complete 24hour urine specimen must be preserved with HCl. 
In healthy adults (24-42 years of age) who have no fluid restrictions and a normal activity level, normal plasma concentration of ADH is 0.35-1.94 ng/L (0.32-1.80 pmol/L). However, such low levels cannot be measured with certainty by most assays. Therefore, for best interpretation of results, plasma osmolality should be correlated with ADH values.  In the presence of nephrogenic DI, plasma ADH levels are usually elevated in relation to plasma osmolality. Conversely, with neurogenic DI, ADH levels decrease as plasma osmolality increases.
Water deprivation test. Results from an overnight water deprivation test will help confirm the presence of DI.  Dehydration strongly stimulates ADH release, which can be assessed indirectly by measuring urine and plasma osmolality or directly by measuring plasma ADH.  If other causes of polyuria, such as diabetes mellitus, psychogenic polydipsia (excess water intake due to a mental disorder), and renal tubule damage, have not yet been ruled out, this test will also help with differentiation diagnosis.  However, before water deprivation begins, the patient should have documentable polyuria (urine volume [greater than] 2.5 L/d), and glycosuria should be excluded. Plasma osmolality should be [greater than or equal to] 295 mmol/L, and serum sodium should be [greater than or equal to] 145 mmol/L. 
The test begins when the patient is weighed in the evening (time is noted), and blood and urine specimens are collected to determine sodium level and osmolality. Substances that influence ADH secretion (nicotine, alcohol, and caffeine) should be avoided, and creatinine excretion can be measured to estimate completeness of the urine collection. No food or drink is allowed until the test ends, but care is taken to ensure that the patient's body weight does not decrease more than 5% during the test and that the patient does not develop symptoms of severe dehydration. [2,21]
After an 8-hour overnight fast, the patient's weight, blood pressure, urine and plasma osmolalities, and urine volume are measured. At this time, healthy subjects generally have a urine osmolality [greater than] 800 mmol/L (see Table 3), and a plasma osmolality that is still within the normal range (with changes [less than] 9 mmol/L). [2,21] For patients with DI, the urine osmolality often remains low (less than that of plasma), and the plasma osmolality is [greater than] 300 mmol/L. [12,21] These values can also be expressed as the urine/plasma (U/P) osmol ratio, which normally ranges from 1-3 when using a random urine sample.  After fluid restriction, this ratio normally increases to a range of 3.0-4.7, but for fluid restricted patients with incomplete or partial neurogenic DI, the ratio will remain [less than] 1. 
Once the urine osmolality stabilizes, (i.e., changes [less than or equal to] 30 mmol/L for 2 consecutive hours, which usually requires 8-12 hours), specimens are collected for plasma osmolality and possibly for plasma ADH  If urine osmolality is [less than or equal to] 400 mmol/L, 5 units of ADH are administered, and urine osmolality is measured 1 hour later. The test is then terminated.
After exogenous ADH, healthy patients still lose [less than or equal to] 3% of their body weight, do not develop increased serum sodium or plasma osmolality, and produce concentrated urine (osmolality greater than or equal to 800 mmol/L) that increases [less than] 9% (see Table 3)  For patients with severe neurogenic DI, the increase in urine osmolality is [greater than] 50%, and the U/P ratio will increase substantially because the kidneys can now respond to ADH, which was missing before administration.  For patients with partial defects in ADH release, the increase in urine osmolality is 10-50% (see Table 3)  For nephrogenic DI, neither the U/P osmol ratio nor urine osmolality increases after ADH administration, because the kidneys cannot respond to this hormone, regardless of its source. [2,13]
Despite assay difficulties, plasma ADH levels from a specimen collected during water deprivation (after urine osmolality stabilizes) can also be used to establish the correct diagnosis in difficult cases. After water deprivation, patients with neurogenic DI have low or inappropriately normal plasma ADH levels relative to a high plasma osmolality. Patients with nephrogenic DI have high plasma levels of ADH when plasma osmolality exceeds 300 mmol/L. If the diagnosis remains unclear, plasma ADH levels could also be measured in response to a 2-hour infusion with hypertonic saline.  The patient could also be evaluated for improvement after receiving desamino-D-arginine vasopressin (DDAVP) every 12 hours for 3 days. 
Drug therapy. The drug of choice for patients with neurogenic DI is a synthetic analog of ADH in the form of aqueous arginine-vasopressin or DDAVP.  Patients with partial neurogenic DI may also benefit from the oral hypoglycemic agent, chlorpropamide, which stimulates the release of ADH from the pituitary gland and augments renal tubule response to ADH.  However, its use is limited because of the associated hypoglycemia. Clofibrate can also stimulate ADH secretion.  At least one study (n = 20) suggests the use of indapamide for partial neurogenic DI,  but this drug requires more studies for confirmation. This and other diuretics can be effective because they interfere with renal diluting capacity.  Patients with nephrogenic DI will not respond to exogenous ADH but also benefit from diuretics, such as thiazide or hydrochlorothiazide, in combination with a sodium-restricted diet. 
Depending on the specific, underlying cause, both neurogenic and nephrogenic DI can be transient or a chronic, lifelong condition. In either case, laboratory data are essential for proper diagnosis and to initiate proper treatment.
For patients with SIADH, the production and release of ADH is autonomous and sustained in the absence of known stimuli.  Various drugs and conditions can precipitate SIADH, but small-cell lung cancer is one of the most common causes. [2,12] This fairly common form of cancer and other cancers, such as melanoma, prostate, and stomach cancer, [25,26] ectopically produce ADH or an ADH-like peptide.  Transient (acute) forms of SIADH may be drug-induced or appear in the postoperative patient, usually producing clinical signs and symptoms for 3-5 days after surgery.  As the US population ages, SIADH may become even more common as an unintended side effect of antidepressant medications. [27,28] A thorough drug history and use of the lowest effective dose can help clinicians effectively manage elderly patients and limit the risk of this adverse drug reaction. Also, electrolytes should be assayed for any elderly person who receives an antidepressant (especially a serotonin reuptake inhibitor) and whose clinic al status suddenly changes.
Clinical signs and symptoms. Patients with SIADH show no clinical evidence of volume depletion, and both renal and adrenal functions are normal. However, they can exhibit hyponatremia, weight gain, diminished urination, and nausea. As hyponatremia progresses, the patient will become either lethargic or restless and combative. Eventually, consciousness decreases, and convulsions and coma may be observed. As with the neurologic changes that accompany hypematremia in DI, if the neurologic changes associated with hyponatretnia in SIADH are left untreated, they can cause permanent brain damage or death.
Although SIADH is one of the most common causes of hyponatremia in hospitalized patients, other disorders can cause hyponatremia and must be differentiated from SIADH. These disorders include congestive heart failure, renal insufficiency, severe bums, nephrotic syndrome, liver cirrhosis, hypothyroidism, and depletional hyponatremia caused by severe diarrhea and vomiting or by excessive sweating. [2,29]
Diagnosis. Whatever the cause, the clinical results are usually the same. When fluid intake is unrestricted, free water reabsorption is increased in the kidney. Serum sodium levels decrease to [less than] 130 mmol/L, and plasma osmolality decreases to [less than] 270 mmol/L.2 Urine output decreases, and as urine becomes more concentrated, its osmolality exceeds 1,200 mmol/L. If plasma and urinary ADH results are obtained, they might reveal that the hormone is inappropriately high in patients with SIADH.  However, for [greater than] 80% of these patients, ADH levels are comparable with those found in normally hydrated, healthy adults due to abnormal, sustained production rather than to dramatically increased production. Therefore, ADH levels in these patients can be recognized as inappropriate only in relation to low plasma osmolalities. 
Water-load test. A water-loading study can also help establish the diagnosis of SIADH. However, water loading is dangerous unless the patient has no symptoms of hyponatremia and has received appropriate treatment to raise serum sodium to a safe level (generally [greater than] 125 mmol/L).  The patient should be supine for the duration because an upright position can produce invalid results by decreasing glomerular filtration. Baseline plasma and urine osmolality are measured, and the patient receives water at 20 mL/kg during a 15- to 30-minute period. Plasma and urine osmolality are measured hourly for the next 4-5 hours. Total urine output is also measured. 
Normally, 90% of the water load is excreted within 4 hours. Plasma osmolality decreases by [greater than or equal to] 5 mmol/L, and urine osmolality decreases to [less than or equal to] 100 mmol/L, producing a U/P ratio [greater than] 1.  In SIADH, [less than] 90% of the water load is excreted, and urine osmolality remains [greater than] 100 mmol/L. Patients with severe SIADH may even excrete [less than] 40% of the water load within 5 hours.  To support the diagnosis, a specimen for plasma ADH may be collected at 90-120 minutes after water loading. 
The main treatment: Fluid restriction. Once the diagnosis of SIADH is confirmed, the underlying cause must be treated, and any drugs contributing to SIADH must be discontinued. Patients with acute or chronic SIADH also require fluid restriction to prevent further hemodilution. The degree of fluid restriction varies, depending on the patient's serum sodium level.
Patients with chronic SIADH and those with acute SIADH who don't respond to water restriction will also receive medication such as furosemide (to increase serum sodium levels) and demeclocycline or fludrocortisone, both of which reduce the response of the renal collecting ducts to ADH.  Occasionally, phenytoin is used because it inhibits the release of ADH from the pituitary gland. Changes in the patient's status or abnormal laboratory results may warrant immediate medical attention.
As with DI, the prognosis in SIADH depends primarily on its underlying cause. Regardless of the cause, timely laboratory data can mean the difference between death from fluid imbalance and the possibility of rapid, full recovery.
Web sites and biotechnology
An online search using "antidiuretic hormone" as a search term yields a variety of Web sites that can provide information about ADH and related pathologies. This information is in addition to that found on MEDLINE. Of particular interest is a commercial application involving the human ADH renal receptor.  A technology group claims to have isolated the human ADH receptor gene and cDNA and to have developed several cell lines that express high levels of this receptor. If confirmed by outside sources, these cell lines would eliminate the need to work with human kidneys and would provide a permanent and easily accessible source for studying this receptor. This is especially important when performing research because the ADH receptor for other species apparently cannot be substituted for the human ADH receptor. Therefore, these cell lines make it easier to develop drugs to treat human ADH pathologies, congestive heart failure, hypotension, and edema.
Charol Abrams is a contract medical writer and editor who develops educational materials primarily for physician CME.
(1.) Austgen L, Bowen RA. Pathophysiology of the endocrine system. Antidiuretic hormone (vasopressin). http://arbl.cvmbs.colostate.edu/ hbooks/pathphys/endocrine/hypopit/adh.html.Accessed 11/15/99.
(2.) Whitley RJ, Meikle AW, Watts NB. Hormones from the posterior lobe of the pituitary gland (Neurohypophyseal hormones). In: Burtis CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. Philadelphia, PA: WB Saunders Company; 1994: p. 1685-1697.
(3.) Nephrogenic diabetes insipidus foundation. NDI terminology-vasopressin. http://www.ndif.org/Terms/vasopressin.html. Accessed 11/15/99.
(4.) Whelton A, Watson AJ, Rock RC. Water homeostasis. In: Burns CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. Philadelphia, PA: W.B. Saunders Company; 1994: p. 1549-1588.
(5.) Pudek MR. Adrenal hormones and hypertension. In: Kaplan LA, Peace AJ, Kazmierezak SC, eds. Clinical Chemistry: Theory, Analysis, and Correlation. St. Louis, MO: Mosby; 1996: p. 912-938.
(6.) First MR. Renal function. In: Kaplan LA, Pesce AJ, Kazmierczak SC, eds. Clinical Chemistry: Theory, Analysis, and Correlation. St. Louis, MO: Mosby; 1996: p. 484-504.
(7.) Toffaltti J. Electolytes. In: Dufour DR, Christenson RH, eds. Course Notes: Professional Practice in Clinical Chemistry: A Review. Washington DC: AACC Press; 1995: p. 559-601.
(8.) Kleinman LI, Lorenz JM. Physiology and pathophysiology of body water and electrolytes. In: Kaplan LA, Pesce AJ, Kazmierczak SC, eds. Clinical Chemistry: Theory, Analysis, and Correlation. St. Louis, MO: Mosby; 1996: p. 439-463.
(9.) Knoers NV, van Os CH. Molecular and cellular defects in nephrogenic diabetes insipidus. Curr Opin Nebrol Hypertens. 1996;5(4):353-358.
(10.) Demers LM. General endocrinology. In: Kaplan LA, Pesce AJ, Kazmierczak SC, eds. Clinical Chemistry: Theory, Analysis, and Correlation. Sr. Louis, MO: Mosby; 1996: p. 849-866.
(11.) Satta A, Varoni MV, Palomba D, Pals A, Demontis R, Anania V. Relationship between cerebrospinal fluid pressure and plasmatic ADH. Pharmacol Res. 1999;39(5):383-388.
(12.) Howanitz JH, Howanitz PJ, Henry JB. Evaluation of endocrine function. In: Henry JB, ed; Nelson DA, Tomar RH, Washington JA II, assoc edo. Clinical Diagnosis and Management by Laboratory Methods. Philadelphia, PA: W.B. Saunders Company; 1991: p. 308-348.
(13.) Preuss HG, Podlasek SJ, Henry JB. Evaluation of renal function and water, electrolyte, and acid-base balance. In: Henry JB, ed; Nelson DA, Tomar RH, Washington JA II, assoc. eds. Clinical Diagnosis and Management by Laboratory Methods. Philadelphia, PA: W.B. Saunders Company; 1991: p. 119-139.
(14.) Siggaard C, Rittig S, Corydon TJ, or al. Clinical and molecular evidence of abnormal processing and trafficking of the vasopressin preprohormone in a large kindred with familial neurohypophyseal diabetes insipidus due to a signal peptide mutation. F Clin Endocrinol Metab. 1999;84(8): 2933-2941.
(15.) Heater DH. If ADH goes out of balance. RN. 1999;62(7):42-50.
(16.) Bichet DG. Nephrogenic diabetes insipidus. Am F Med. 1998;105(5): 431-442.
(17.) Dods RF. Diabetes mellitus. In: Kaplan LA, Pesce AJ, Kazmierczak SC eds. Clinical Chemistry: Theory, Analysis, and Correlation. Sr. Louis, MO: Mosby; 1996: p. 613-641.
(18.) Manual of laboratory, X-ray and special procedures. The New York Hospital Cornell Medical Center. Antidiuretic hormone, plasma. http://mfonet.med.cornell.edu/lab/eescs/A_Antidiuretic_Hormone_Plasma .htm. Accessed 11/15/99.
(19.) Inter Science Institute C.U.R.E. Handbook. Antidiuretic hormone (ADH, vasopressin). http://www.interscilsa.com/book/indi11.html. Accessed 11/15/99.
(20.) USCD Healthcare, Laboratory Services Guide, Clinical Laboratories, University of California, San Diego. http://health.ucsd.edu/labref/P223.html. Accessed 11/15/99.
(21.) Nephrology Service, Walter Reed Army Medical Center, HSHL-MN (Nephrology), Water Deprivation Teat. http://www.wrame/amedd.army.mil/ departments/medicine/nephro.../water_deprivation_test.cf. Accessed 11/15/99.
(22.) Davis BB, Zenser TV. Evaluation of renal concentrating and diluting ability. In: Preuss HG, ed. Clinics in Laboratory Medicine. Philadelphia, PA: W.B. Saunders; 1993: p. 131-134.
(23.) Tetiker T, Sort M, Kocak M. Efficacy of indapamide in central diabetes insipidus. Arch Intern Med. 1999;159(17):2085-2087.
(24.) Welch JJ. Pediatric endocrinology, Diabetes Insipidus. Georgetown University. http://gucfm.georgetown.edu/welchjj/netscut/endocrinology/diabetes_in sipidus.html. Accessed 11/15/99.
(25.) Lo Scocco G, Di Lernia V, Bisighini G. Syndrome of inappropriate secretion of antidiuretic hormone in a patient affected by metastatic melanoma. Melanoma Res. 1998;8(4):367-369.
(26.) Mouallem M, Ela N, Segal-Lieberman G. Meningeal carcinomatosis and syndrome of inappropriate antidiuretic hormone in a patient with metastatic carcinoma of the stomach. South Med J. 1998;91(11): 1076-1078.
(27.) Pollock BG. Adverse reactions of antidepressants in elderly patients. J Clin Psychiatry. 1999;Suppl 20:4-8.
(28.) Severe adverse reaction: Paroxetine-induced acute hyponatremia. Nurses Drug Alert. 1999;23(7):54.
(29.) DeVita MV, Michelis MF. Perturbations in sodium balance. In: Preuss HG, ed. Clinics in Laboratory Medicine. Philadelphia, PA: W.B. Saunders; 1993: p. 135-138.
(30.) Fuhrman SA, Whitley RJ. Child with nausea and vomiting eight days post-craniotomy. In: Tietz NW, Conn RB, Pruden EL, eds. Applied Laboratory Medicine. Philadelphia, PA: W.B. Saunders; 1992: p. 385-391.
(31.) TechExchange Online. Clone of the human antidiuretic hormone receptor and cells expressing the vector (BCM7). http://www.teonline.com/teotech/tr_32891.html. Accessed 1/15/99.
Relationship between changes in ADH levels and various physiologic and laboratory parameters Renal collecting duct As ADH... reabsorption of water... Urine volume... increases  increases decreases decreases  decreases increases Plasma As ADH... Urine osmolality ... osmolality... increases  increases decreases decreases  decreases increases (1.)Osmolality reflects concentration. (2.)Chronic excess becomes syndrome of inappropriate antidiuretic hormone. (3.)Chronic decreased production or effect becomes diabetes insipidus. ADH = antidiuretic hormone. DI versus SIADH: Values or changes in selected laboratory tests  Test DI Serum sodium [greater than] 145 mmol/L Plasma osmolality [greater than] 295 mm/L  Urine osmolality [less than] 300 mmol/L 300-800 mmol/L  U/P osmol ratio [less than] 1 Urine output [greater than] 2.5L/d Test SIADH Normal  Serum sodium [less than] 130 mmol/L 135-145 mmol/L Plasma osmolality [less than] 275 mmol/L 278-298 mmol/L Urine osmolality [greater than] 1,200 mmol/L 50-1,200 mmol/L  U/P osmol ratio [greater than] 3-4 3-4 Urine output decreased approximately 2.5 L/d 
(1.)To suggest a diagnosis, laboratory values must be evaluated collectively and in conjunction with physical exam and signs and symptoms.
(2.)Exact normal values vary with each laboratory.
(3.)With access to drinking water, values are at the high end of normal to slight increase.
(4.)Partial neurogenic DI.
(5.)Varies with food and drink.
(6.)Under normal, nonstressful conditions.
DI = diabetes insipidus; SIADH = syndrome of inappropriate antidiuretic hormone; U/P = urine/plasma.
Values or changes in selected laboratory tests for DI after water restriction  After water restriction alone Laboratory test Normal reponse DI Plasma osmolality Normal range with [greater than] 300 [less than] 9 mmol/L change Urine osmolality [greater than] 800 mmol/L Less than plasma value ([greater than] 300 mmol/L) [less than] 9% increase U/P ratio 3.0-4.7 [greater than] 1.0 After water restriction and ADH administration Laboratory test Normal response Plasma osmolality Normal range with [less than] 5 mmol/L change Urine osmolality [greater than] 800 mmol/L with U/P ratio 3.0-4.7 Laboratory test DI Plasma osmolality Dramatic decrease  Slight decrease  No change  Urine osmolality [greater than] 50% increase  10-50% increase  No change  U/P ratio Increase [2,3] No change  (1.)See Table 2 for baseline normal values. (2.)Neurogenic DI. (3.)Partial neurogenic DI. (4.)Nephrogenic DI. DI = diabetes insipidus; ADH = antidiuretic hermone.
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|Publication:||Medical Laboratory Observer|
|Date:||Feb 1, 2000|
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