Release and Decay Kinetics of Copeptin vs AVP in Response to Osmotic Alterations in Healthy Volunteers.
Journal article

Release and Decay Kinetics of Copeptin vs AVP in Response to Osmotic Alterations in Healthy Volunteers.

  • Fenske WK Leipzig University Medical Center, Integrated Center for Research and Treatment Adiposity Diseases, Leipzig, Germany.
  • Schnyder I Department of Endocrinology, Diabetology, and Metabolism, University Hospital of Basel, Basel, Switzerland.
  • Koch G Pediatric Pharmacology and Pharmacometrics, University Children's Hospital of Basel, Basel, Switzerland.
  • Walti C Department of Endocrinology, Diabetology, and Metabolism, University Hospital of Basel, Basel, Switzerland.
  • Pfister M Pediatric Pharmacology and Pharmacometrics, University Children's Hospital of Basel, Basel, Switzerland.
  • Kopp P Division of Endocrinology, Metabolism, and Molecular Medicine and Center for Genetic Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
  • Fassnacht M Division of Endocrinology and Diabetes, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany.
  • Strauss K Division of Endocrinology and Diabetes, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany.
  • Christ-Crain M Department of Endocrinology, Diabetology, and Metabolism, University Hospital of Basel, Basel, Switzerland.
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  • 2017-12-22
Published in:
  • The Journal of clinical endocrinology and metabolism. - 2018
English Context
Copeptin is the C-terminal fragment of the arginine vasopressin (AVP) prohormone whose measurement is more robust than that of AVP. Similar release and clearance characteristics have been suggested promoting copeptin as a surrogate marker.


Objective
To characterize the physiology of osmotically regulated copeptin release and its half-life in direct comparison with plasma AVP.


Design
Ninety-one healthy volunteers underwent a standardized three-phase test protocol including (1) osmotic stimulation into the hypertonic range by hypertonic-saline infusion followed by osmotic suppression via (2) oral water load and (3) subsequent glucose infusion. Plasma copeptin, AVP, serum sodium, and osmolality levels were measured in regular intervals.


Results
In phase 1, an increase in median osmotic pressure [289 (286; 291) to 311 (309; 314) mOsm/kg H2O] caused similar release kinetics of plasma copeptin [4 (3.1; 6) to 29.3 (18.6; 48.2) pmol/L] and AVP [1 (0.7; 1.6) to 10.3 (6.8; 18.8) pg/mL]. Subsequent osmotic suppression to 298 (295; 301) mOsm/kg at the end of phase 3 revealed markedly different decay kinetics between both peptides-an estimated initial half-life of copeptin being approximately 2 times longer than that of AVP (26 vs 12 minutes).


Conclusion
Copeptin is released in equimolar amounts with AVP in response to osmotic stimulation, suggesting its high potential as an AVP surrogate for differentiation of osmotic disorders. Furthermore, we here describe the decay kinetics of copeptin in response to osmotic depression enabling to identify a half-life for copeptin in direct comparison with AVP.
Language
  • English
Open access status
bronze
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/273312
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