title: Copeptin, a surrogate marker of vasopressin, is associated with accelerated renal function decline in renal transplant recipients.
abstract: BACKGROUND
  Chronically elevated vasopressin (VP) plasma levels have been shown to induce accelerated renal function decline in rats with chronic renal failure. Whether endogenous VP is a renal risk factor in humans has not been investigated yet. We aimed to investigate whether, in renal transplant recipients, VP concentration is associated with change in renal function during follow-up.
  
  
  METHODS
  In this prospective study, all consecutive patients visiting our kidney transplant outpatient clinic between August 2001 and July 2003 were asked to participate. Serum creatinine was assessed at baseline and at follow-up. Copeptin, the C-terminal portion of the precursor of VP, was determined at baseline (immunoassay). Univariate and multivariate regression analyses were performed to investigate the association between copeptin and renal function decline.
  
  
  RESULTS
  Overall, 548 patients were included 6.0 (2.8-11.6) years after transplantation (men 54%, age 52 [43-60] years). Median follow-up was 3.2 (2.7-3.7) years. Median copeptin level was 9.1 (5.0-18.6) pmol/L at baseline. Copeptin was significantly associated with change in estimated Glomerular Filtration Rate (eGFR; MDRD) during follow-up. When our study population was subdivided according to gender-stratified tertiles of increasing copeptin concentration, mean changes in eGFR during follow-up were -0.03, -0.44, and -1.06 mL/min/1.73 m2 per year. In multivariate regression analysis, the association of copeptin at baseline with change in eGFR during follow-up remained significant after adjustment for age, gender, baseline eGFR, and known risk factors for renal function decline.
  
  
  CONCLUSIONS
  These findings suggest that in renal transplant patients, VP may play a role in renal function decline.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
authors.forename: Esther
authors.initials: E
authors.lastname: Meijer
authors.forename: Stephan J L
authors.initials: SJ
authors.lastname: Bakker
authors.forename: Paul E
authors.initials: PE
authors.lastname: de Jong
authors.forename: Jaap J
authors.initials: JJ
authors.lastname: Homan van der Heide
authors.forename: Willem J
authors.initials: WJ
authors.lastname: van Son
authors.forename: Joachim
authors.initials: J
authors.lastname: Struck
authors.forename: Simon P M
authors.initials: SP
authors.lastname: Lems
authors.forename: Ron T
authors.initials: RT
authors.lastname: Gansevoort
mesh_terms: D000328:Adult; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D005919:Glomerular Filtration Rate; D006020:Glycopeptides / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000503:physiopathology; D016030:Kidney Transplantation / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D011446:Prospective Studies; D051381:Rats; D014667:Vasopressins / Q000502:physiology
chemical_list: D015415:Biomarkers; D006020:Glycopeptides; C048197:copeptins; D014667:Vasopressins