Robert Lewis

Early in the coronavirus-2019 (COVID-19) containment strategy, people with end-stage renal disease (ESRD) were identified as extremely clinically vulnerable and subsequently asked to ‘shield’ at home where possible. The aim of this study was to investigate how these restrictions and the transition to an increased reliance on telemedicine within clinical care of people living with kidney disease impacted the physical activity (PA), wellbeing and quality of life (QoL) of adults dialysing at home (HHD) or receiving in-centre haemodialysis (ICHD) in the UK. Individual semistructured telephone interviews were conducted with adults receiving HHD (n = 10) or ICHD (n = 10), were transcribed verbatim and, subsequently, thematically analysed. As result of the COVID-19 restrictions, PA, wellbeing and QoL of people with ESRD were found to have been hindered. However, widespread support for the continued use of telemedicine was strongly advocated and promoted independence and satisfaction in patient care. These findings highlight the need for more proactive care of people with ESRD if asked to shield again, as well as increased awareness of safe and appropriate PA resources to help with home-based PA and emotional wellbeing.

There is a lack of consensus about how early chronic kidney disease (CKD) should be diagnosed and managed in older people. Some believe that reduced renal function in older age is usually benign and that identifying it as a condition requiring medical intervention is inappropriate, whereas others believe it represents an important public health issue. This uncertainty is not reflected in management guidelines. There is no controversy, however, that advanced CKD is particularly dangerous in older people. They are at risk of acute kidney injury, often worsened by unenlightened medical management. As CKD advances towards end stage in older people, treatment choices are even more difficult to make and there is a need for insightful input from carers to optimise outcomes.

Chronic kidney disease (CKD) is now recognized as a major public health issue. One consequence of this condition is disturbance of mineral and bone homeostasis. Bone disease (renal osteodystrophy) as a consequence of CKD has long been recognized. However, it is now appreciated that the mineral and bone disturbances of CKD (and perhaps treatment of them) lead to vascular calcification, which is a cause of significant morbidity. In recognition of the widespread nature of the condition, the term CKD-mineral bone disorder (CKD-MBD) is now in general use to describe the biochemical, skeletal and vascular changes that occur in CKD. The pathogenesis of CKD-MBD is incompletely understood but has recently been redefined with the emergence of fibroblast growth factor 23 (FGF-23) as a major influence on control of vitamin D and parathyroid hormone. This review describes the classification of CKD and current understanding of the mechanisms underlying CKD-MBD (incorporating FGF-23). It describes and evaluates the means of identifying CKD-MBD in the clinical setting and the interventions available for treatment. It then reviews current clinical guidelines for the use of biochemical markers in clinical decision-making. In acknowledgement of the paucity of evidence upon which these guidelines are based, areas where clinical research might be directed in the future will be identified.