After you receive the kit, store the lyophilized components and standard diluent at -20°C for up to one year from the kit's assembly date. The remaining components should be stored in the refrigerator (4 - 8°C) also up to 1 year. Long term storage, improper storage conditions and large temperature fluctuation cycles may cause precipitates in the TMB solution and in the ELISA buffer concentrate. These precipitates should not affect the assay noticeably. Nevertheless, if you observe such precipitates, we recommend to avoid them by allowing them to sink to the bottom.
Detection Range
0-500ng/ml
General Description
Copeptin is a 39 amino acid peptide generated by the cleavage of Vasopressin-neurophysin 2-copeptin. The main stimuli for copeptin are similar to arginine vasopressin (AVP), that is an increase in osmolality and a decrease in arterial blood volume and pressure. Copeptin has been evaluated as a diagnostic biomarker in vasopressin-dependent disorders of body fluid homeostasis, that is diabetes insipidus and syndrome of inappropriate thirsting (SIAD), respectively. Baseline copeptin levels, without prior thirsting, identify patients with nephrogenic diabetes insipidus. This ELISA was developed with serum from rabbits immunized with Copeptin coupled to a carrier protein.
Standard Curve
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Background
Copeptin is part of the precursor molecule of arginine vasopressin (AVP) released by the pituitary gland and has been found to be strongly associated with diseases such as diabetes and coronary heart disease. The AVP precursor molecule is a polypeptide consisting of 164 amino acids divided into four parts, namely the N-terminal signal peptide, AVP, neurophysin II and copeptin. AVP, neurophysin II and copeptin are co-stored in neurohypophysis vesicles before being secreted.
Figure 1. The synthesis of copeptin and AVP (Source: Săcărescu A, et al. 2021)
AVP, also known as antidiuretic hormone, effectively promotes vasoconstriction, regulates the body's osmotic pressure, keeps the cardiovascular system stable, and maintains hemodynamic as well as endo-environmental stability. The AVP precursor molecule generates AVP, copeptin and neurophysin II, of which AVP and copeptin are released into the blood in equimolar amounts. Thus, blood copeptin levels can reflect AVP release levels. Plasma AVP has the disadvantages of too small molecular weight, short half-life and instability, and its stable detection is more difficult, while copeptin is more stable in vivo and easy to be detected, so it is expected to be used to replace AVP for assisting in clinical diagnosis and evaluating the severity of the disease.
Copeptin is more responsive to immediate neurological stress triggers, rising and falling rapidly within hours of injury, aiding in the early diagnosis and assessment of cardiovascular disease. Investigators found that testing troponin in conjunction with copeptin improved the diagnostic sensitivity and negative predictive value of non-ST-segment elevation myocardial infarction, but the specificity and accuracy were reduced. On the other hand, diabetic cardiovascular disease is the most serious and prevalent complication in diabetic patients. Analysis of coronary artery calcification scores in diabetic patients revealed that the more severe the coronary artery lesion and the greater the number of diseased branches, the higher the plasma copeptin level. It has even been shown that copeptin is also more sensitive and specific than myoglobin in diagnosing myocardial injury. Copeptin's efficacy in diagnosing acute myocardial infarction (AMI) within 2 h of the onset of acute chest pain was superior to that of cTnI, and plasma copeptin levels were significantly higher in patients with AMI than in those with unstable angina.
References
1. Săcărescu A, et al. Role of copeptin in the diagnosis of traumatic neuroendocrine dysfunction. Neuropeptides. 2021 Oct;89:102167.
2. Mu D, et al. Copeptin as a Diagnostic and Prognostic Biomarker in Cardiovascular Diseases. Front Cardiovasc Med. 2022 Jul 4;9:901990.
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References
Classical and Delayed Orthostatic Hypotension in Patients With Unexplained Syncope and Severe Orthostatic Intolerance
Background: Orthostatic hypotension (OH) is a major sign of cardiovascular autonomic failure leading to orthostatic intolerance and syncope. Orthostatic hypotension is traditionally divided into classical OH (cOH) and delayed OH (dOH), but the differences between the two variants are not well-studied. We performed a systematic clinical and neuroendocrine characterization of OH patients in a tertiary syncope unit. Methods: Among 2,167 consecutive patients (1,316 women, 60.7%; age, 52.6 +/- 21.0 years) evaluated for unexplained syncope and severe orthostatic intolerance with standardized cardiovascular autonomic tests including head-up tilt (HUT), we identified those with a definitive diagnosis of cOH and dOH. We analyzed patients' history, clinical characteristics, hemodynamic variables, and plasma levels of epinephrine, norepinephrine, C-terminal-pro-arginine-vasopressin (CT-proAVP), C-terminal-endothelin-1, mid-regional-fragment of pro-atrial-natriuretic-peptide and pro-adrenomedullin in the supine position and at 3-min HUT. Results: We identified 248 cOH and 336 dOH patients (27% of the entire cohort); 111 cOH and 152 dOH had blood samples collected in the supine position and at 3-min HUT. Compared with dOH, cOH patients were older (68 vs. 60 years, p < 0.001), more often male (56.9 vs. 39.6%, p < 0.001), had higher systolic blood pressure (141 vs. 137 mmHg, p = 0.05), had lower estimated glomerular filtration rate (73 vs. 80 ml/min/1.73 m(2), p = 0.003), more often pathologic Valsalva maneuver (86 vs. 49 patients, p < 0.001), pacemaker-treated arrhythmia (5 vs. 2%, p = 0.04), Parkinson's disease (5 vs. 1%, p = 0.008) and reported less palpitations before syncope (16 vs. 29%, p = 0.001). Supine and standing levels of CT-proAVP were higher in cOH (p = 0.022 and p < 0.001, respectively), whereas standing norepinephrine was higher in dOH (p = 0.001). After 3-min HUT, increases in epinephrine (p < 0.001) and CT-proAVP (p = 0.001) were greater in cOH, whereas norepinephrine increased more in dOH (p = 0.045). Conclusions: One-quarter of patients with unexplained syncope and severe orthostatic intolerance present orthostatic hypotension. Classical OH patients are older, more often have supine hypertension, pathologic Valsalva maneuver, Parkinson's disease, pacemaker-treated arrhythmia, and lower glomerular filtration rate. Classical OH is associated with increased vasopressin and epinephrine during HUT, but blunted increase in norepinephrine.
The predictive value of stable precursor fragments of vasoactive peptides in patients with chronic heart failure: data from the GISSI-heart failure (GISSI-HF) trial
Aims Though various neurohormonal systems are concurrently activated during heart failure (HF), their biological effectors are not always easy to measure due to their short life in vivo, instability in biological samples, or very low concentrations. We measured the plasma concentrations of four stable precursor fragments of neurohormonal systems in patients with chronic HF and evaluated their relationship with outcome. Methods and results This study was performed in 1237 patients with chronic and stable HF enrolled in the GISSI-heart failure trial (GISSI-HF). The following four precursor fragments, mid-regional pro-atrial natriuretic peptide (MR-proANP), mid-regional pro-adrenomedullin (MR-proADM), C-terminal pro-endothelin-1 (CT-proET-1) and C-terminal pro-vasopressin (CT-proAVP or copeptin), were measured at randomization and after 3 months. Baseline concentrations were independent predictors of clinical outcome (median follow-up 3.9 years). The addition of MR-proANP improved net reclassification for mortality when added to multivariable models based on clinical risk factors alone [net reclassification improvement (NRI) = 0.12, P = 0.0007] or together with NT-proBNP (NRI = 0.06, P = 0.01). Changes in MR-proANP concentrations were related to mortality [HR (95% CI) 1.38 (0.99-1.93), P = 0.0614 and 1.58 (1.13-2.21), P = 0.0078 in the middle and highest vs. lowest tertiles], while changes in the other markers were not. Conclusion In patients with chronic and stable HF enrolled in a multicentre, randomized, clinical trial, measurement of stable precursor fragments of vasoactive peptides provided prognostic information independent of natriuretic peptides which are currently the best biomarkers for risk stratification.
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Figure 1. The synthesis of copeptin and AVP
