Mineral and bone disorders in chronic kidney disease: new insights into mechanism and management.
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.
Wessex Renal and Transplant Service, Queen Alexandra Hospital, Portsmouth PO6 3LY, UK. Robert.lewis@porthosp.nhs.uk
Robert
R
Lewis
D015415:Biomarkers / Q000097:blood; D001851:Bone Diseases, Metabolic / Q000150:complications* / Q000628:therapy; D019468:Disease Management; D000089703:Fibroblast Growth Factor-23; D006801:Humans; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000628:therapy
D015415:Biomarkers; C000717427:FGF23 protein, human; D000089703:Fibroblast Growth Factor-23