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Abstract
Chronic kidney disease is associated with an accelerated risk of cardiovascular (CV) mortality. Seminal work over the last decade has identified abnormal bone metabolism as an important modulator of the increased CV burden in this cohort. In particular, FGF23, a phosphaturic hormone with serum levels found to be markedly elevated in chronic kidney disease, is independently associated with increased risks of all-cause mortality and CV events. This editorial will discuss the proposed mechanisms linking FGF23 to CV disease in chronic kidney disease, namely, direct cardiac myocyte toxicity, endothelial dysfunction and vascular calcification.
Financial & competing interests disclosure
D Johnson is a consultant for Baxter Healthcare Pty Ltd and has previously received research funds from this company. D Johnson has also received speakers’ honoraria and research grants from Fresenius Medical Care and is a recipient of a Queensland Government Health Research Fellowship. C Hawley has received research funding from Baxter Healthcare Pty Ltd, Shire Pty Limited and Fresenius Medical Care. C Hawley has received travel grants from Amgen Australia. R Krishnasamy has received speaking honoraria from Shire Australia. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.