Chronic kidney disease

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