期刊
NEPHROLOGY DIALYSIS TRANSPLANTATION
卷 36, 期 3, 页码 405-412出版社
OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfz196
关键词
bone fractures; CKD; MBD; phosphate levels
This review discusses the central role of phosphate in the pathogenesis of CKD-MBD and its association with fracture risk, both in hyperphosphatemia and hypophosphatemia.
In chronic kidney disease (CKD), phosphate homoeostasis plays a central role in the development of mineral and bone disorder (MBD) together with decreased serum calcium and elevated serum parathyroid hormone, fibroblast growth factor 23 and sclerostin levels. Today there are only a few data exploring the direct role of abnormal phosphate homoeostasis and hyperphosphataemia in the development of CKD-MBD. On the other hand, several studies have looked at the link between hyperphosphataemia and cardiovascular morbidity and mortality in CKD, but there is a lack of evidence to indicate that lowering phosphate levels improves cardiovascular outcomes in this population. Furthermore, the impact of liberalizing phosphate targets on CKD-MBD progression and bone fracture is currently not known. In this review we discuss the central role of phosphate in the pathogenesis of CKD-MBD and how it may be associated with fracture risk, both in hyper- and hypophosphataemia.
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