Marta Christov1. 1. aDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center bDivision of Endocrinology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Abstract
PURPOSE OF REVIEW: To review the emerging literature on changes in fibroblast growth factor 23 (FGF23) levels in the setting of acute kidney injury (AKI). RECENT FINDINGS: Studies suggest that FGF23 levels are elevated in patients with AKI and correlate with increased risk of death or need for dialysis in adults, or prolonged ventilation time and higher fluid gain in children. Animal studies have shown that the cause behind this FGF23 increase is multifactorial and includes increased production in bone and decreased clearance, but not vitamin D or parathyroid hormone (PTH) activated pathways. Interestingly, FGF23 levels are 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 AKI need to be confirmed in larger cohorts and evaluated for long-term outcomes such as the development of new chronic kidney disease (CKD) or CKD progression, as well as cardiovascular disease, similar to the studies of FGF23 in the prevalent CKD population. SUMMARY: FGF23 levels are elevated in patients with AKI and are associated with morbidity and mortality in 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.
PURPOSE OF REVIEW: To review the emerging literature on changes in fibroblast growth factor 23 (FGF23) levels in the setting of acute kidney injury (AKI). RECENT FINDINGS: Studies suggest that FGF23 levels are elevated in patients with AKI and correlate with increased risk of death or need for dialysis in adults, or prolonged ventilation time and higher fluid gain in children. Animal studies have shown that the cause behind this FGF23 increase is multifactorial and includes increased production in bone and decreased clearance, but not vitamin D or parathyroid hormone (PTH) activated pathways. Interestingly, FGF23 levels are 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 AKI need to be confirmed in larger cohorts and evaluated for long-term outcomes such as the development of new chronic kidney disease (CKD) or CKD progression, as well as cardiovascular disease, similar to the studies of FGF23 in the prevalent CKD population. SUMMARY:FGF23 levels are elevated in patients with AKI and are associated with morbidity and mortality in 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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