title: Copeptin levels and kidney function in ADPKD: case-control study.
abstract: BACKGROUND
  Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease. Studies have suggested a possible prognostic role of copeptin in determining the rate of progressive kidney function decline in ADPKD patients. However, it remains unresolved whether the changes in copeptin levels are specific for ADPKD or merely reflect a decline in glomerular filtration rate (GFR) regardless of the etiology of chronic kidney disease (CKD).
  
  
  METHODS
  We performed a case-control study in ADPKD and non-ADPKD (control) patients. Patients were categorized based on the GFR-category (G-stage, KDIGO). We evaluated urea, creatinine, cystatin C, and copeptin in plasma and correlated these levels with estimated glomerular filtration rate (eGFR) (CKD-EPI). All p-values were two sided, and p < 0.05 was considered as statistically significant.
  
  
  RESULTS
  We enrolled 112 ADPKD and 112 control patients. The median copeptin level was 10.72 (interquartile range (IQR) 5.21 - 26.21) pmol/L in the ADPKD group and 12.32 (IQR 4.47 - 30.73) pmol/L in the control group. The median copeptin level increased according to the G-stage in a progressive fashion and remained statistically significant across all G-stages and in both groups. Copeptin levels were not significantly different between ADPKD and control groups. We found a significant inverse correlation between copeptin level and eGFR (Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)) in the ADPKD, r = -0.81 (p < 0.001), and in the control group, r = -0.76 (p < 0.001).
  
  
  CONCLUSIONS
  Copeptin levels seem to be strongly correlated with renal function rather than the presence of ADPKD. Further prospective studies need to evaluate its role as a prognostic marker in the early stage of CKD for ADPKD progression.
authors.forename: Valentina
authors.initials: V
authors.lastname: Corradi
authors.forename: Francesca
authors.initials: F
authors.lastname: Martino
authors.forename: Fiorella
authors.initials: F
authors.lastname: Gastaldon
authors.forename: Elisa
authors.initials: E
authors.lastname: Scalzotto
authors.forename: Carlotta
authors.initials: C
authors.lastname: Caprara
authors.forename: Antonio
authors.initials: A
authors.lastname: Fortunato
authors.forename: Giulia
authors.initials: G
authors.lastname: Pinaffo
authors.forename: Cristina
authors.initials: C
authors.lastname: Marchetti
authors.forename: Francesca
authors.initials: F
authors.lastname: Fabbi
authors.forename: Davide
authors.initials: D
authors.lastname: Giavarina
authors.forename: Fiorenza
authors.initials: F
authors.lastname: Ferrari
authors.forename: Mitchell H
authors.initials: MH
authors.lastname: Rosner
authors.forename: Claudio
authors.initials: C
authors.lastname: Ronco
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003404:Creatinine / Q000097:blood*; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology*; D006020:Glycopeptides / Q000097:blood*; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood* / Q000503:physiopathology; D011379:Prognosis; D011446:Prospective Studies
chemical_list: D015415:Biomarkers; D006020:Glycopeptides; C048197:copeptins; D003404:Creatinine