26144 Copeptin proAVP, Plasma (CPAVP)

​The investigation of the differential diagnosis of patients with water balance disorders, including Diabetes Insipidus (DI) in conjunction with osmolality and hydration status.

May aid in the evaluation of cardiovascular disease in conjunction with other cardiac markers.

​Gross hemolysis

Sepsis, severe sepsis, septic shock, lower respiratory tract infections, chronic obstructive pulmonary disease (COPD), and cardiovascular diseases, ie, chronic heart failure may increase copeptin concentrations.

Arginine vasopressin (AVP) receptor antagonist therapies and other diseases in which AVP has been shown to play an important pathophysiologic role may also increase copeptin concentration.

In some cases bronchial carcinoma may lead to ectopic copeptin secretion.

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

Some patients who have been exposed to animal antigens, either in the environment or as part of treatment or imaging procedures, may have circulating antianimal antibodies present. These antibodies may interfere with the assay reagents to produce unreliable results.

Arginine vasopressin (AVP) and copeptin (also known as copeptin proAVP or copeptin AVP) are derived from the same precursor peptide. Copeptin has been proposed as a more stable, potentially superior, surrogate marker of AVP in the assessment of water balance disorders. Unlike AVP, copeptin is stable in plasma. Both copeptin and AVP are responsive to osmotic stimuli and increase in response to water deprivation. In healthy subjects, water deprivation causes the plasma osmolality to rise above approximately 280-290 mOsmol/kg, leading to the release of AVP and copeptin into the circulation. Copeptin increases gradually with fasting and water deprivation and declines rapidly after intake of water and/or food.

Diabetes insipidus (DI) is characterized by the inability to appropriately concentrate urine in response to volume and osmolar stimuli. The main causes for DI are decreased AVP production (central DI) or decreased renal response to AVP (nephrogenic DI).

The determination of the underlying disease pathology in patients with polyuria and altered plasma osmolality is often difficult. Polyuria can be related to insufficient AVP (central DI), reduced sensitivity to AVP (nephrogenic DI), or excessive water intake. Measurement of plasma copeptin concentration has been shown to be useful in the investigation of these AVP-related disorders. Additionally, utilization of copeptin has been proposed in the assessment of syndrome of inappropriate antidiuretic (SIADH).

Copeptin is also a marker of acute hemodynamic stress, and has been reported to aid in the prognosis or diagnosis of several cardiac disorders such as acute coronary syndrome, stable coronary artery disease, congestive heart failure, and acute ischemic stroke. Some studies have demonstrated that copeptin may improve prediction of mortality and heart disease outcome when combined with natriuretic peptides such as B-type natriuretic peptide (BNP) and N-terminal pro b-type natriuretic peptide (NT-proBNP).