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J Am Soc Nephrol. 2014 Oct;25(10):2376-83. doi: 10.1681/ASN.2013080895. Epub 2014 Apr 10.

A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis.

Author information

1
Department of Internal Medicine I, Endocrine and Diabetes Unit, University Hospital Würzburg, Würzburg, Germany; Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany; Leipzig University Medical Center, IFB Adiposity Diseases, Leipzig, Germany;
2
Division of Endocrinology, University Hospitals, Basel, Switzerland;
3
Department of Internal Medicine I, Endocrine and Diabetes Unit, University Hospital Würzburg, Würzburg, Germany;
4
Pediatric Endocrinology, University Children's Hospital Basel, University Basel, Basel, Switzerland;
5
Department of Internal Medicine I, Endocrine and Diabetes Unit, University Hospital Würzburg, Würzburg, Germany; Department of Internal Medicine IV, Ludwig-Maximilians-Universität, Munich, Germany;
6
University Clinic for Internal Medicine, Kantonsspital Baselland-Bruderholz, Bruderholz, Switzerland; and.
7
Department of Physiology and Medicine, Hôpital du Sacré-Coeur, Université de Montréal, Montréal, Canada.
8
Department of Internal Medicine I, Endocrine and Diabetes Unit, University Hospital Würzburg, Würzburg, Germany; Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany;
9
Department of Internal Medicine I, Endocrine and Diabetes Unit, University Hospital Würzburg, Würzburg, Germany; Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany; wiebkekristin.fenske@medizin.uni-leipzig.de allolio_b@ukw.de.

Abstract

Hyponatremia, the most frequent electrolyte disorder, is caused predominantly by the syndrome of inappropriate antidiuresis (SIAD). A comprehensive characterization of SIAD subtypes, defined by type of osmotic dysregulation, is lacking, but may aid in predicting therapeutic success. Here, we analyzed serial measurements of serum osmolality and serum sodium, plasma arginine vasopressin (AVP), and plasma copeptin concentrations from 50 patients with hyponatremia who underwent hypertonic saline infusion. A close correlation between copeptin concentrations and serum osmolality existed in 68 healthy controls, with a mean osmotic threshold±SD of 282±4 mOsM/kg H2O. Furthermore, saline-induced changes in copeptin concentrations correlated with changes in AVP concentrations in controls and patients. With use of copeptin concentration as a surrogate measure of AVP concentration, patients with SIAD could be grouped according to osmoregulatory defect: Ten percent of patients had grossly elevated copeptin concentrations independent of serum osmolality (type A); 14% had copeptin concentrations that increased linearly with rising serum osmolality but had abnormally low osmotic thresholds (type B); 44% had normal copeptin concentrations independent of osmolality (type C), and 12% had suppressed copeptin concentrations independent of osmolality (type D). A novel SIAD subtype discovered in 20% of patients was characterized by a linear decrease in copeptin concentrations with increasing serum osmolality (type E or "barostat reset"). In conclusion, a partial or complete loss of AVP osmoregulation occurs in patients with SIAD. Although the mechanisms underlying osmoregulatory defects in individual patients are presumably diverse, we hypothesize that treatment responses and patient outcomes will vary according to SIAD subtype.

PMID:
24722436
PMCID:
PMC4178436
DOI:
10.1681/ASN.2013080895
[Indexed for MEDLINE]
Free PMC Article
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