Copeptin, a Surrogate Marker of Vasopressin, Is Associated with Disease Severity in Autosomal Dominant Polycystic Kidney Disease

Esther Meijer, Stephan J. L. Bakker, Eric J. van der Jagt, Gerjan Navis, Paul E. de Jong, Joachim Struck, Ron T. Gansevoort*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

64 Citations (Scopus)

Abstract

Background and objectives Experimental studies suggest a detrimental role for vasopressin in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). However, it is unknown whether endogenous vasopressin concentration is associated with disease severity in patients with ADPKD.

Design, setting, participants, & measurements Plasma copeptin concentration (a marker of endogenous vasopressin levels) was measured in 102 ADPKD patients (diagnosis based on Ravine criteria) by an immunoassay. Plasma and urinary osmolarity were also measured. To assess disease severity, GFR and effective renal blood flow were measured by continuous infusion of I-125-iothalamate and I-131-hippuran, total renal volume by magnetic resonance imaging, and 24-hour urinary albumin excretion by nephelometry.

Results In these ADPKD patients, copeptin was associated with the various markers of disease severity in ADPKD (positively with total renal volume [R = 0.47] and albuminuria [R = 0.39] and negatively with GFR [R = -0.58] and effective renal blood flow [R = -0.52], all P <0.001). These associations were independent of age, gender, and use of diuretics. Copeptin was furthermore associated with plasma osmolarity (P <0.001) but not with 24-hour urinary volume, 24-hour urinary osmolarity or fractional urea excretion (P = 0.7, 0.9, and 0.3, respectively).

Conclusions On cross-sectional analysis, copeptin is associated with disease severity in ADPKD patients, supporting the results of experimental studies that suggest that vasopressin antagonists have a renoprotective effect in ADPKD and offering a good prospect for clinical studies with these agents. Clin J Am Soc Nephrol 6: 361-368, 2011. doi: 10.2215/CJN.04560510

Original languageEnglish
Pages (from-to)361-368
Number of pages8
JournalClinical Journal of the American Society of Nephrology
Volume6
Issue number2
DOIs
Publication statusPublished - Feb-2011

Keywords

  • GLOMERULAR-FILTRATION-RATE
  • RENAL CONCENTRATING CAPACITY
  • WATER-INTAKE
  • RECEPTOR ANTAGONISTS
  • ANTIDIURETIC ACTION
  • VOLUME PROGRESSION
  • EPITHELIAL-CELLS
  • PLASMA-FLOW
  • FAILURE
  • RATS

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