01760nas a2200205   4500000000100000008004100001100001400042700001300056700001700069700001700086700001100103700001300114700001900127245012600146250001500272300001200287490000700299520120200306020004601508       2012                            d1 aHawley C.1 aBadve S.1 aToussaint N.1 aPedagogos E.1 aTan S.1 aElder G.1 aPerkovic Vlado00aPhosphate in early chronic kidney disease: Associations with clinical outcomes and a target to reduce cardiovascular risk  a2012/05/12  a433-4440 v173 a<p>
There is an intimate association between mineral and bone disorders in chronic kidney disease (CKD) and the extensive burden of cardiovascular disease (CVD) in this population. High phosphate levels in CKD have been associated with increased all-cause mortality and cardiovascular morbidity and mortality. Observational studies have also shown a consistent relationship between serum phosphate in the normal range and all-cause and cardiovascular mortality, left ventricular hypertrophy (LVH) and decline in renal function. Furthermore, fibroblast growth factor-23 (FGF-23), a phosphaturic hormone, increases very early in the course of CKD and is strongly associated with death and CVD, including LVH and vascular calcification. Few studies have addressed outcomes using interventions to reduce serum phosphate in a randomized controlled fashion; however, strategies to address cardiovascular risk in early CKD are imperative and phosphate is a potential therapeutic target. This review outlines the epidemiological and experimental evidence highlighting the relationship between excess phosphate and adverse outcomes, and discusses clinical studies required to address this problem.
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