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Clinical Science (2017) 131, 225–226 doi: 10.

1042/CS20160624

Chronic kidney disease


Christian Delles* and Raymond Vanholder†

*Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8TA, U.K.
†Nephrology Section, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium

Key words: chronic kidney disease, cardiovascular disease, fibrosis, translational science

Chronic kidney disease (CKD) is characterized by persist- gical and molecular studies as well as novel unbiased approaches
ing renal damage and/or loss of renal function. The condition is to pathway discovery such as proteomics, transcriptomics and
associated with high morbidity and mortality throughout the con- metabolomics, and RNA sequencing and whole exome sequen-
tinuum from early disease to advanced stages that require renal cing as new technologies applied to the problem of identifying
replacement therapy. Although much progress has been made in the molecular basis for CKD.
prevention, detection and treatment, CKD remains a major public Patients with CKD benefit from a multidisciplinary approach.
health problem. Its global prevalence is estimated at 5–10% and, The high prevalence of CKD exposes all clinical specialities to
primarily because of cardiovascular morbidity and mortality, the patients with impaired renal function where expert nephrological
global burden of CKD-associated diseases is alarmingly high [1]. advice is often required to inform treatment decisions. Likewise,
The scope of Clinical Science is to translate molecular bios- many forms of CKD are the result of diabetes, hypertension,
cience and experimental research into medical insights. CKD is autoimmune conditions and infectious diseases where nephro-
a prime example of a disease in need of a truly translational ap- logists benefit from the knowledge of experts in other areas of
proach that unravels pathophysiological mechanisms to develop medicine in order to offer the best possible treatment to their pa-
new diagnostic, preventative and therapeutic strategies for the tients. This multidisciplinarity of CKD is ideally suited to Clinical
benefit of patients at risk of or with overt CKD. The editors have Science and something we hope this call for papers will reflect.
therefore decided to launch a call for papers on CKD that address Of course, Clinical Science does not want to “compete” with
disease mechanisms and their translation into clinical practice. specialist journals in renal medicine and we would therefore par-
We are honoured to oversee the editorial handling of submissions ticularly welcome submissions of translational research papers
to this series and look forward to seeing some of the best research and reviews that span from renal to other medical disciplines.
in this area of Clinical Science. In order to attract the highest quality research, it is import-
We would expect papers in this series to have both a molecular ant to outline which papers will not be suitable for the special
and a clinical angle, these being tightly connected. Clearly, there series. Clinical Science does generally not publish the results
are numerous translational aspects in CKD. The molecular mech- of clinical trials of investigational products and there will be
anisms linking pathogenetic factors with persistent renal damage no exception to this rule for this series. Similarly, work that is
are manifold and incompletely understood; improved knowledge purely focused on physiology or pathophysiology in experimental
of disease mechanisms will translate to better treatment of pa- models but without translational clinical potential is unlikely to
tients with CKD. The immediate sequelae of CKD such as an- be considered. Biomarker studies and genetic association studies
aemia, uraemia and altered calcium and phosphate homoeostasis that do not unravel disease mechanisms may also be better placed
are clinically well known although their pathogenesis is still not in other journals.
entirely clear; the recent recognition of factors such as fibroblast We have already opened the series with contributions pub-
growth factor-23 (FGF23) as important regulators of phosphate lished in recent editions of the journal. We would like to high-
homoeostasis is a prominent example of novel pathophysiological light the review of Cobo et al. [6] on sex and gender differences in
insights with potential to impact on management of patients with CKD; a study by Coughlan et al. [7] on changes in mitochondrial
CKD [2]. And although the relationship of CKD with cardiovas- dynamics and function in the development of diabetic nephro-
cular diseases is also well known, it remains unclear how exactly pathy and the review by Holterman et al. [8] on the role the Nox
renal diseases increase cardiovascular risk; peculiarities in pa- family of enzymes in the pathogenesis of renal diseases. A paper
tients with CKD such as the lack of a protective effect of statins by Xu et al. [9] is of particular interest for this series as it describes
in patients with end-stage renal disease [3,4] and specific pat- the development of CKD from acute kidney injury and how the
terns of myocardial damage not typically seen in patients with transcription cofactor yes-associated protein (YAP) is involved
normal renal function [5] are examples of areas that require more in regeneration towards normal renal function or progression to
mechanistic work. Such work may include traditional physiolo- CKD following the acute injury. The journal is very interested in

Abbreviations: CKD; chronic kidney disease

Correspondence: Professor Christian Delles (email Christian.Delles@glasgow.ac.uk)


C 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society. 225
C. Delles and R. Vanholder

studies into regeneration on the one hand and remodelling and 4 Wanner, C., Krane, V., März, W., Olschewski, M., Mann, J.F., Ruf,
fibrosis/fibrogenesis on the other hand and the study by Xu et al. G., Ritz, E., German Diabetes and Dialysis Study Investigators
(2005) Atorvastatin in patients with type 2 diabetes mellitus
[9] addresses both aspects in a rat model and in human biopsy undergoing hemodialysis. N. Engl. J. Med. 353, 238–248
samples. CrossRef PubMed
We decided to write this editorial in order to remind the com- 5 Mark, P.B., Johnston, N., Groenning, B.A., Foster, J.E., Blyth, K.G.,
munity of the call for papers that addresses this priority research Martin, T.N., Steedman, T., Dargie, H.J. and Jardine, A.G. (2006)
Redefinition of uremic cardiomyopathy by contrast-enhanced
area. Having seen the success of these first submissions to the cardiac magnetic resonance imaging. Kidney Int. 69, 1839–1845
series, we are excited to receive further excellent submissions in CrossRef PubMed
the field of CKD in the near future. 6 Cobo, G., Hecking, M., Port, F.K., Exner, I., Lindholm, B.,
Stenvinkel, P. and Carrero, J.J. (2016) Sex and gender differences
in chronic kidney disease: progression to end-stage renal disease
and haemodialysis. Clin. Sci. (Lond.) 130, 1147–1163
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Received 14 October 2016/22 November 2016; accepted 29 November 2016


Version of Record published 5 January 2017, doi: 10.1042/CS20160624

226 
C 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

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