Abstract
BackgroundFibroblast growth factor-23 (FGF-23), a novel regulator of mineral metabolism, is markedly elevated in chronic kidney disease and has been associated with poor long-term outcomes. However, whether FGF-23 has an analogous role in acute kidney injury is unknown. The goal of this study was to measure FGF-23 levels in critically ill patients with acute kidney injury to determine whether FGF-23 levels were elevated, as in chronic kidney disease.MethodsPlasma FGF-23 and intact parathyroid hormone (PTH) levels were measured in 12 patients with acute kidney injury and 8 control subjects.ResultsFGF-23 levels were significantly higher in acute kidney injury cases than in critically ill subjects without acute kidney injury, with a median FGF-23 level of 1948 RU/mL (interquartile range (IQR), 437-4369) in cases compared with 252 RU/mL (IQR, 65-533) in controls (p = 0.01). No correlations were observed between FGF-23 and severity of acute kidney injury (defined by the Acute Kidney Injury Network criteria); among patients with acute kidney injury, FGF-23 levels were higher in nonsurvivors than survivors (median levels of 4446 RU/mL (IQR, 3455-5443) versus 544 RU/mL (IQR, 390-1948; p = 0.02). Severe hyperparathyroidism (defined as intact PTH >250 mg/dL) was present in 3 of 12 (25%) of the acute kidney injury subjects versus none of the subjects without acute kidney injury, although this result did not meet statistical significance.ConclusionsWe provide novel data that demonstrate that FGF-23 levels are elevated in acute kidney injury, suggesting that FGF-23 dysregulation occurs in acute kidney injury as well as chronic kidney disease. Further studies are needed to define the short- and long-term clinical effects of dysregulated mineral metabolism in acute kidney injury patients.
Highlights
Acute kidney injury (AKI) is the most common reason for inpatient nephrology consultation and is associated with in-hospital mortality rates of 45-70% [1,2]
We studied 12 cases who developed at least Stage I AKI and 8 control subjects who did not
There was a correlation between parathyroid hormone (PTH) and Fibroblast growth factor-23 (FGF-23) levels (r = 0.55, p = 0.02); when this analysis was restricted to patients with AKI, this correlation only had borderline statistical significance (r = 0.58, p = 0.05), likely due to the small size of the cohort. In this cross-sectional case series, we report for the first time that critically ill patients with AKI due to causes other than rhabdomyolysis have elevated FGF-23 levels compared with critically ill controls
Summary
Acute kidney injury (AKI) is the most common reason for inpatient nephrology consultation and is associated with in-hospital mortality rates of 45-70% [1,2]. Changes commonly found in CKD patients–anemia, acid/base dysregulation, Dysregulated mineral metabolism, including derangements in calcium and phosphate levels, is relatively well characterized in CKD, and correction of hypocalcemia, vitamin D deficiency, and hyperphosphatemia in CKD patients is standard-of-care [11,12,13] These derangements are all associated with an increased risk of death and cardiovascular outcomes in patients with CKD and end-stage renal disease [14,15,16,17,18,19,20,21,22]. Fibroblast growth factor-23 (FGF-23), a novel regulator of mineral metabolism, is markedly elevated in chronic kidney disease and has been associated with poor long-term outcomes. The goal of this study was to measure FGF-23 levels in critically ill patients with acute kidney injury to determine whether FGF-23 levels were elevated, as in chronic kidney disease
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