Tasneem M, Mannix C, Wong A, Zhang J, Rangan G. Is serum copeptin a modifiable biomarker in autosomal dominant polycystic kidney disease? World J Nephrol 2018; 7(2): 51-57 [PMID: 29527508 DOI: 10.5527/wjn.v7.i2.51]
Corresponding Author of This Article
Gopala Rangan, FRACP, MBBS, PhD, Associate Professor, Staff Nephrologist, Centre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road (PO Box 412), Westmead, Sydney 2145, Australia. g.rangan@sydney.edu.au
Research Domain of This Article
Clinical Neurology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Nephrol. Mar 6, 2018; 7(2): 51-57 Published online Mar 6, 2018. doi: 10.5527/wjn.v7.i2.51
Is serum copeptin a modifiable biomarker in autosomal dominant polycystic kidney disease?
Moomal Tasneem, Carly Mannix, Annette Wong, Jennifer Zhang, Gopala Rangan
Moomal Tasneem, Carly Mannix, Annette Wong, Jennifer Zhang, Gopala Rangan, Centre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, Sydney 2145, Australia
Moomal Tasneem, Carly Mannix, Annette Wong, Jennifer Zhang, Gopala Rangan, Department of Renal Medicine, Westmead Hospital, Sydney 2145, Australia
Author contributions: Tasneem M contributed to draft the manuscript, review the literature and the content; Mannix C contributed to draft the manuscript and contributed to the content; Wong A contributed to draft the manuscript and the content; Zhang J contributed to draft the manuscript and contributed to the content; Rangan G contributed to draft the manuscript, review the literature and contributed to the content.
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported. Rangan G is recipient of an investigator initiated grant from the Danone Nutricia Research (manufacturer of bottled water).
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Gopala Rangan, FRACP, MBBS, PhD, Associate Professor, Staff Nephrologist, Centre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road (PO Box 412), Westmead, Sydney 2145, Australia. g.rangan@sydney.edu.au
Telephone: +61-2-86273502
Received: December 18, 2017 Peer-review started: December 18, 2017 First decision: January 23, 2018 Revised: January 29, 2018 Accepted: February 28, 2018 Article in press: February 28, 2018 Published online: March 6, 2018
Abstract
The availability of disease-modifying drugs for the management of autosomal dominant polycystic kidney disease (ADPKD) has accelerated the need to accurately predict renal prognosis and/or treatment response in this condition. Arginine vasopressin (AVP) is a critical determinant of postnatal kidney cyst growth in ADPKD. Copeptin (the C-terminal glycoprotein of the precursor AVP peptide) is an accurate surrogate marker of AVP release that is stable and easily measured by immunoassay. Cohort studies show that serum copeptin is correlated with disease severity in ADPKD, and predicts future renal events [decline in renal function and increase in total kidney volume (TKV)]. However, serum copeptin is strongly correlated with creatinine, and its additional value as a prognostic biomarker over estimated glomerular filtration rate and TKV is not certain. It has also been suggested that copeptin could be a predictive biomarker to select ADPKD patients who are most likely to benefit from AVP-modifying therapies, but prospective data to validate this assumption are required. In this regard, long-term randomised clinical trials evaluating the effect of prescribed water intake on renal cyst growth may contribute to addressing this hypothesis. In conclusion, although serum copeptin is aligned with the basic pathogenesis of ADPKD, further rigorous studies are needed to define if it will contribute to enabling the delivery of personalised care in ADPKD.
Core tip: Serum copeptin is correlated with disease severity in autosomal dominant polycystic kidney disease (ADPKD), and predicts future renal events (decline in renal function and increase in total kidney volume). The aim of this review is to critically evaluate the role of copeptin as a prognostic biomarker of renal outcomes in ADPKD, and if it has potential as a predictive marker of treatment response.
