Curr Opin Nephrol Hypertens 2014[Jul]; 23 (4): 340-5 PMID24848938show ga
Purpose of review: to review emerging literature on changes in fibroblast growth factor 23 (FGF23) levels in the setting of acute kidney injury. Recent findings: studies suggest that FGF23 levels are elevated in patients with acute kidney injury, and correlate with increased risk of death or need for dialysis (in adults) or prolonged ventilation time and higher fluid gain (in children). Animal work shows that the etiology behind this FGF23 increase is multi-factorial and includes increased production in bone and decreased clearance, but not vitamin D or PTH-activated pathways. Interestingly, FGF23 levels were found to be mildly elevated even in hospitalized patients without kidney injury, although this observation may be limited to only c-terminal FGF23 fragments. The prognostic implications of an elevated FGF23 value in patients with acute kidney injury need to be confirmed in larger cohorts and evaluated for long-term outcomes such as development of new CKD or CKD progression, as well as cardiovascular disease, similar to studies of FGF23 in the prevalent CKD population. Summary: FGF23 levels are elevated in patients with AKI and are associated with morbidity and mortality is small human studies. Mechanistic work in animals suggests that the elevation is independent of PTH or vitamin D-signaling pathways. Much work remains to understand the physiology behind FGF23 elevation and the long-term effects of FGF23 in AKI.
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Curr+Opin+Nephrol+Hypertens 2014 ; 23 (4): 340-5
