title: Relationship of copeptin, a surrogate marker for arginine vasopressin, with change in total kidney volume and GFR decline in autosomal dominant polycystic kidney disease: results from the CRISP cohort.
abstract: BACKGROUND
  Experimental studies indicate that arginine vasopressin (AVP) may have deleterious effects in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). However, the significance of AVP in human ADPKD is unclear.
  
  
  METHODS
  Longitudinal observational study with 8.5 (IQR, 7.7-9.0) years' follow-up (CRISP [Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease]).
  
  
  METHODS
  241 patients with ADPKD with creatinine clearance >70 mL/min.
  
  
  METHODS
  Plasma copeptin concentration, a surrogate marker for AVP.
  
  
  RESULTS
  Change in measured glomerular filtration rate (mGFR, assessed by iothalamate clearance) and total kidney volume (measured by magnetic resonance imaging).
  
  
  METHODS
  Baseline copeptin level, plasma and urinary osmolality, and measurements of total kidney volume and mGFR during follow-up.
  
  
  RESULTS
  In these patients (median age, 34 [IQR, 25-40] years; 38% men; median mGFR, 94 [IQR, 79-145] mL/min/1.73 m(2); median total kidney volume, 859 [IQR, 577-1,299] mL), median copeptin level was 2.9 (IQR, 1.8-5.1) pmol/L. Copeptin was not associated with plasma osmolality (P = 0.3), the physiologic stimulus for AVP release, but was associated significantly with change in total kidney volume during follow-up (P < 0.001). This association remained significant after adjusting for sex, age, cardiovascular risk factors, and diuretic use (P = 0.03). Copeptin level was associated borderline significantly with change in mGFR after adjusting for these variables (P = 0.09).
  
  
  CONCLUSIONS
  No standardization of hydration status at time of copeptin measurement.
  
  
  CONCLUSIONS
  These data show that in ADPKD, copeptin level, as a marker for AVP, is not correlated with plasma osmolality. Most importantly, high copeptin levels are associated independently with disease progression in early ADPKD. This is in line with experimental studies that indicate a disease-promoting role for AVP.
authors.affiliation: Department of Nephrology, University Medical Center Groningen, University of Groningen, 9700 RB, Groningen, the Netherlands.
authors.forename: Wendy E
authors.initials: WE
authors.lastname: Boertien
authors.forename: Esther
authors.initials: E
authors.lastname: Meijer
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: James E
authors.initials: JE
authors.lastname: Bost
authors.forename: Joachim
authors.initials: J
authors.lastname: Struck
authors.forename: Michael F
authors.initials: MF
authors.lastname: Flessner
authors.forename: Ron T
authors.initials: RT
authors.lastname: Gansevoort
authors.forename: Vicente E
authors.initials: VE
authors.lastname: Torres
mesh_terms: D000328:Adult; D001127:Arginine Vasopressin; D015415:Biomarkers / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D006020:Glycopeptides / Q000097:blood*; D006801:Humans; D007668:Kidney / Q000473:pathology* / Q000503:physiopathology*; D008137:Longitudinal Studies; D008297:Male; D009929:Organ Size; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D055815:Young Adult
chemical_list: D015415:Biomarkers; D006020:Glycopeptides; C048197:copeptins; D001127:Arginine Vasopressin