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

Debbie Zittema, Wendy E. Boertien, Andre P. van Beek, Robin P. F. Dullaart, Casper F. M. Franssen, Paul E. de Jong, Esther Meijer, Ron T. Gansevoort*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Background 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

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. Clin J Am Soc Nephrol 7: 906-913, 2012. doi: 10.2215/CJN.11311111

Original languageEnglish
Pages (from-to)906-913
Number of pages8
JournalClinical Journal of the American Society of Nephrology
Volume7
Issue number6
DOIs
Publication statusPublished - Jun-2012

Keywords

  • URINE CONCENTRATION
  • ANTIDIURETIC-HORMONE
  • CHILDREN
  • PROLIFERATION
  • ANTAGONISTS
  • INHIBITION
  • CELLS

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