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Changes in Plasma Copeptin, the C-Terminal Portion of Arginine Vasopressin during Water Deprivation and Excess in Healthy Subjects

Division of Endocrinology, Diabetology, and Clinical Nutrition (G.S., B.M., U.K., M.C.-C.), University Hospital, CH-4031 Basel, Switzerland; Pediatric Endocrinology and Diabetology (G.S.), University Children’s Hospital, CH-4005 Basel, Switzerland; Research Department (N.G.M., J.S.), B.R.A.H.M.S. AG, D-16761 Hennigsdorf/Berlin, Germany; and Clinic of Endocrinology, Diabetes, and Clinical Nutrition (K.B.), University Hospital, CH-8091 Zurich, Switzerland

Address all correspondence and requests for reprints to: Dr. Gabor Szinnai, Pediatric Endocrinology and Diabetology, University Children’s Hospital Basel, Römergasse 8, CH-4005 Basel, Switzerland. E-mail: gabor.szinnai{at}unibas.ch.

Context: The measurement of arginine vasopressin (AVP) is often cumbersome because it is unstable with a short half-life time. AVP is derived from a larger precursor peptide along with the more stable peptide copeptin. Copeptin is the C-terminal part of provasopressin and has been shown to be a useful tool to indicate AVP concentration in critically ill patients.

Objective: The objective of the study was to evaluate the clinical usefulness of copeptin as a new marker in disordered states of blood volume and plasma osmolality.

Design and Setting: This was a prospective observational study in a university hospital.

Participants and Main Outcome Measures: Three techniques with respective control studies were used in 24 healthy adults to produce changes in plasma osmolality and/or volume: 1) a 28-h water deprivation, 2) a 17-h hypertonic saline infusion combined with thirsting, and 3) a hypotonic saline infusion with iv desmopressin administration during free water intake.

Results: Water deprivation produced a weight loss of 1.7 kg, an increase in plasma osmolality to 294.8 ± 4.3 mosmol/kg, and an increase of copeptin from 4.6 ± 1.7 pmol/liter to 9.2 ± 5.2 pmol/liter (P < 0.0001). During hypertonic saline infusion and thirsting with a raise of plasma osmolality to 296.1 ± 3.4 mosmol/kg, copeptin increased from 4.9 ± 3.0 pmol/liter to 19.9 ± 4.8 pmol/liter (P < 0.0001). Conversely, during hypotonic saline infusion, plasma osmolality decreased to 271.3 ± 4.1 mosmol/kg, and copeptin decreased from 6.2 ± 2.4 pmol/liter to 2.4 ± 2.1 pmol/liter (P < 0.01).

Conclusion: Copeptin shows identical changes during disordered water states as previously shown for AVP. It might be a reliable marker of AVP secretion and substitute for the measurement of circulating AVP levels in clinical routine.

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				W. Fenske, S. Stork, A. Blechschmidt, S. G. K. Maier, N. G. Morgenthaler, and B. Allolio Copeptin in the Differential Diagnosis of Hyponatremia J. Clin. Endocrinol. Metab., January 1, 2009; 94(1): 123 - 129. [Abstract] [Full Text] [PDF]