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Kidney Week

Abstract: TH-PO850

AD(H)PKD-Copeptin as Biomarker in Patients with Autosomal-Dominant Polycystic Kidney Disease (ADPKD)

Session Information

Category: Genetic Diseases of the Kidneys

  • 1001 Genetic Diseases of the Kidneys: Cystic

Authors

  • Oehm, Simon, Department 2 of Internal Medicine, Renal Division; University of Cologne, Cologne, Germany
  • Arjune, Sita, Department 2 of Internal Medicine, Renal Division; University of Cologne, Cologne, Germany
  • Burst, Volker Rolf, Department 2 of Internal Medicine, Renal Division; University of Cologne, Cologne, Germany
  • Benzing, Thomas, Department 2 of Internal Medicine, Renal Division; University of Cologne, Cologne, Germany
  • Grundmann, Franziska, Department 2 of Internal Medicine, Renal Division; University of Cologne, Cologne, Germany
  • Mueller, Roman-Ulrich, Department 2 of Internal Medicine, Renal Division; University of Cologne, Cologne, Germany
Background

Prediction of disease progression in ADPKD is a challenging task. While there are established biomarkers such as total kidney volume (TKV), the identification of new and easily obtainable biomarkers is required to facilitate both prognostic assessment and patient selection regarding targeted therapy. Moreover, new biomarkers would ideally allow the prediction of long-term treatment responses. Post-hoc analyses of the TEMPO 3:4 study showed that copeptin could be one of those biomarkers. We investigated copeptin as a possible new biomarker in participants of the AD(H)PKD study.

Methods

Copeptin was tested in serum samples from patients of the AD(H)PKD study. These were collected and analyzed at first presentation as well as at follow-up visits. In total, we collected copeptin values from 369 patients, 54 of these during treatment with Tolvaptan. Copeptin values were analysed for both, their distribution in different patient groups (e.g. age, Mayo Class) as well as their response to Tolvaptan treatment.

Results

Copeptin values from 315 patients without tolvaptan treatment were significantly lower than copeptin values from patients receiving tolvaptan (8.65 pmol/l vs. 19.74 pmol/l; p < 0.0001). A consistent trend towards higher copeptin values with increasing stages of chronic kidney disease (CKD) was observed in both groups. This trend also applied for increasing TKV. Patients receiving tolvaptan showed higher copeptin values than patients without Tolvaptan treatment in all stages of CKD as well as all Mayo classes. In 8 patients longitudinal copeptin measurements prior to tolvaptan administration and on a dose of 90/30mg were available and revealed a significant increase after start of tolvaptan treatment (copeptin before tolvaptan: 5,6 pmol/l, copeptin while receiving tolvaptan 21,25 pmol/l; p=0.0007).

Conclusion

Our findings in the real-life setting are in line with the results from the post-hoc analysis of the TEMPO 3:4 study. Copeptin may serve as a new biomarker in ADPKD regarding both disease progression and response to tolvaptan treatment. Future analyses regarding disease outcome in correlation to copeptin will help to support the use of copeptin as an easily obtainable biomarker in daily clinical routine.