Copeptin in the Differential Diagnosis of the Polydipsia-Polyuria Syndrome—Revisiting the Direct and Indirect Water Deprivation Tests

Fenske, Wiebke; Quinkler, Marcus; Lorenz, Daniela; Zopf, Kathrin; Haagen, U; Papassotiriou, Jana; Pfeiffer, Andreas F. H.; Faßnacht, Martin; Störk, Stefan; Allolio, Bruno

doi:10.1210/jc.2010-2345

Cited by 150 publications

(112 citation statements)

References 23 publications

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“…The threshold level of ,2 pmol/L for copeptin suppression derives from previous data demonstrating that patients with neurogenic diabetes insipidus and complete AVP deficiency reveal copeptin levels constantly ,2 pmol/L. 8 Finally, patients showing a linear decline in plasma copeptin response to increasing serum osmolality (i.e., a negative copeptin slope below 20.25 pmol/L/mOsM/kg H 2 O; Figure 2, E and F) were classified as having a type E defect. A careful clinical and biochemical re-evaluation of patient records before hypertonic saline infusion revealed no evidence of baseline hypovolemia in this group (Supplemental Table 2).…”

Section: Baseline Characteristics Of Patients With Siad and Healthy Cmentioning

confidence: 99%

A Copeptin-Based Classification of the Osmoregulatory Defects in the Syndrome of Inappropriate Antidiuresis

Fenske

Christ‐Crain

Hörning

et al. 2014

Journal of the American Society of Nephrology

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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 threshold6SD of 28264 mOsM/kg H 2 O. 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.

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Section: Baseline Characteristics Of Patients With Siad and Healthy Cmentioning

confidence: 99%

A Copeptin-Based Classification of the Osmoregulatory Defects in the Syndrome of Inappropriate Antidiuresis

Fenske

Christ‐Crain

Hörning

et al. 2014

Journal of the American Society of Nephrology

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“…According to the standard criteria, a water deprivation test (19,20) is considered normal when urine osmolality is .800 mOsm/kg at plateau. Complete central nephrogenic diabetes insipidus can be expected in patients with urine osmolality ,300 mOsm/kg at plateau and a .50% increase in urine osmolality after DDAVP administration.…”

Section: Interpretation Of a Water Deprivation Testmentioning

confidence: 99%

Vasopressin, Copeptin, and Renal Concentrating Capacity in Patients with Autosomal Dominant Polycystic Kidney Disease without Renal Impairment

Zittema¹,

Boertien²,

Beek

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent hereditary renal disease, characterized by cyst formation in the kidneys leading to end stage kidney failure. It is clinically acknowledged that ADPKD patients have impaired urine concentrating capacity, but the mechanism behind this observation is unknown.Design, setting, participants, & measurements Fifteen ADPKD patients (estimated GFR $60 ml/min per 1.73 m 2 ) and 15 age-and sex-matched healthy controls underwent a standard prolonged water deprivation test in which urine and plasma osmolality, vasopressin, and copeptin were measured. The effect of a synthetic vasopressin analog (desmopressin) injected at the moment of maximal urine concentrating capacity was also studied.Results After 14 hours of water deprivation, ADPKD patients tended to have higher plasma osmolality (P=0.07) and significantly higher vasopressin and copeptin levels (both P,0.05), whereas urine osmolality was similar in ADPKD patients and controls (710 versus 742 mOsmol/kg; P=0.61). Maximal urine concentrating capacity was lower in ADPKD patients (758 versus 915 mOsmol/kg in controls; P,0.001). At maximal urine concentrating capacity, plasma osmolality, vasopressin, and copeptin levels were significantly higher in ADPKD patients. The median increase in urine osmolality after desmopressin administration in ADPKD patients was less than in healthy controls.Conclusions Already early in their disease, ADPKD patients have impaired maximal urine concentrating capacity brought out upon dehydration, with no evidence of impaired hypothalamic response. To maintain fluid balance, vasopressin concentration increases, which is hypothesized to play a role in ADPKD disease progression.

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“…Copeptin measurement holds great promise as a marker of poor prognosis in several acute conditions , in the diagnosis of diabets insipidus [4] and in early rule-out of acute myocardial infarction [5,7]. However, several studies have used copeptin assays with an unacceptable analytical precision at the proposed cut-off values [5,9].…”

Section: Discussionmentioning

confidence: 99%

“…The development of automated copeptin methods now allows for measurement of the release of vasopressin in different disease states [3]. The most direct application for copeptin measurement is in the diagnosis of central diabetes insipidus, a disease caused by a primary vasopressin synthesis defect [4]. Measurement of copeptin has also been suggested in the early exclusion of acute myocardial infarction among patients with suspected acute coronary syndrome [5,6,10].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of a Sensitive Copeptin Assay for Clinical Measurement

Terzic¹,

Johansson-Fällgren²,

Ragnarsson³

et al. 2012

TOCCHEMJ

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Abstract:Background: Copeptin, a marker of vasopressin production, has been introduced for earlier diagnosis of acute myocardial infarction and other clinical emergencies. We evaluated the analytical performance of a new generation copeptin assay in an inter-laboratory trial.Methods: Precision, linearity range, carry-over contamination, the limit of blank and an inter-laboratory comparison trial for the copeptin US KRYPTOR assay were performed on the B·R·A·H·M·S KRYPTOR compact PLUS.Results: The intra-assay imprecision (CVs) was 12.6-2.2% and total imprecision over five days was 12.3-4.3% between 3.1 and 18.2 pmol/L. The assay had excellent linearity between 7-222 pmol/L. The limit of blank was 2.5 pmol/L and the limit of detection was 3.2 pmol/L, but was dependent on the analyte-free material used. No significant difference between sample type, such as serum or different types of plasma or reagent lots, was noted. The copeptin results remained unchanged upon five repeated freeze-thaw cycles. A set of patient samples with a mean copeptin concentration of 2.1-61 pmol/L run at two separate sites showed close correlation (r 2 =0.99, slope=1.01, intercept=0.35), indicating comparable results across laboratories. Conclusion:The new ultrasensitive copeptin KRYPTOR assay shows excellent inter-lab precision, opening up the possibility for international guidelines to exclude acute myocardial infarction.

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Copeptin in the Differential Diagnosis of the Polydipsia-Polyuria Syndrome—Revisiting the Direct and Indirect Water Deprivation Tests

Abstract: Copeptin holds promise as a diagnostic tool in the polyuria-polydipsia syndrome, improving significantly the diagnostic accuracy of the direct WDT.

Cited by 150 publications

References 23 publications

A Copeptin-Based Classification of the Osmoregulatory Defects in the Syndrome of Inappropriate Antidiuresis

A Copeptin-Based Classification of the Osmoregulatory Defects in the Syndrome of Inappropriate Antidiuresis

Vasopressin, Copeptin, and Renal Concentrating Capacity in Patients with Autosomal Dominant Polycystic Kidney Disease without Renal Impairment

Evaluation of a Sensitive Copeptin Assay for Clinical Measurement

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