LAUSR

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 physiolo-