• DOI:10.1093/ndt/gfs070
• Corpus ID: 2803130

Copeptin, a surrogate marker for vasopressin, is associated with kidney function decline in subjects with autosomal dominant polycystic kidney disease.

@article{Boertien2012CopeptinAS,
  title={Copeptin, a surrogate marker for vasopressin, is associated with kidney function decline in subjects with autosomal dominant polycystic kidney disease.},
  author={Wendy E. Boertien and E. Meijer and Debbie Zittema and Marjan A van Dijk and Ton J. Rabelink and Martijn H. Breuning and Joachim Struck and Stephan J. L. Bakker and Dorien J. M. Peters and Paul E. de Jong and Ron T. Gansevoort},
  journal={Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association},
  year={2012},
  volume={27 11},
  pages={
          4131-7
        }
}

• W. Boertien, E. Meijer, +8 authors R. Gansevoort
• Published 1 November 2012
• Medicine
• Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

BACKGROUND
Experimental studies have suggested that vasopressin plays a detrimental role in autosomal dominant polycystic kidney disease (ADPKD). It is, however, unknown whether endogenous vasopressin concentration is associated with kidney function decline in subjects with ADPKD.

METHODS
We measured plasma copeptin (a marker of vasopressin) in 79 ADPKD subjects with renal function assessed during short-term follow-up by inulin clearance measured glomerular filtration rate (mGFR) and during long-term follow-up by Modification of Diet in Renal Disease (MDRD) equation estimated GFR (eGFR).

RESULTS
In these subjects (43% male, age 36.8 ± 10.1 years, GFR 96.8 ± 18.2 mL/min/1.73 m(2)), median copeptin concentration at baseline was 2.71 [interquartile ranges (IQR) 1.63-5.46] pmol/L. Baseline copeptin concentration was inversely associated both with change in mGFR during follow-up for 3.3 (3.1-3.5) years, (R = -0.300, P = 0.01), as well as with change in eGFR during follow-up for 11.2 (4.5-14.3) years, (R = -0.302, P < 0.01). These associations were independent of age, gender and baseline GFR. Nine subjects started renal replacement therapy during follow-up of which eight had at baseline a copeptin concentration above the median in this population.

CONCLUSION
In ADPKD subjects, a higher copeptin concentration is associated with kidney function decline during follow-up, suggesting that copeptin may be a new marker to predict kidney outcome in ADPKD.