title: Vasopressin, copeptin, and renal concentrating capacity in patients with autosomal dominant polycystic kidney disease without renal impairment.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
authors.affiliation: Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
authors.forename: Debbie
authors.initials: D
authors.lastname: Zittema
authors.forename: Wendy E
authors.initials: WE
authors.lastname: Boertien
authors.forename: André P
authors.initials: AP
authors.lastname: van Beek
authors.forename: Robin P F
authors.initials: RP
authors.lastname: Dullaart
authors.forename: Casper F M
authors.initials: CF
authors.lastname: Franssen
authors.forename: Paul E
authors.initials: PE
authors.lastname: de Jong
authors.forename: Esther
authors.initials: E
authors.lastname: Meijer
authors.forename: Ron T
authors.initials: RT
authors.lastname: Gansevoort
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003894:Deamino Arginine Vasopressin / Q000008:administration & dosage; D018450:Disease Progression; D005260:Female; D006020:Glycopeptides / Q000097:blood*; D006801:Humans; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D007671:Kidney Concentrating Ability / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009426:Netherlands; D009481:Neurophysins / Q000097:blood*; D009994:Osmolar Concentration; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood* / Q000503:physiopathology* / Q000652:urine; D011498:Protein Precursors / Q000097:blood*; D012044:Regression Analysis; D013997:Time Factors; D014667:Vasopressins / Q000097:blood*; D014868:Water Deprivation; D014882:Water-Electrolyte Balance; D055815:Young Adult
chemical_list: C438657:AVP protein, human; D015415:Biomarkers; D006020:Glycopeptides; D009481:Neurophysins; D011498:Protein Precursors; C048197:copeptins; D014667:Vasopressins; D003894:Deamino Arginine Vasopressin