Introduction: Elevated FGF-23 serum levels are induced by hyperphosphatemia and are linked to poor skeletal mineralization and adverse outcomes including vascular calcification and mortality. Recently, it was shown that FGF-23 levels are substantially elevated in acute kidney injury (AKI), and that higher levels in AKI are associated with a greater risk of adverse outcomes.
Methods: In 25 vitamin D deficient (25(OH)D <20 ng/ml) critically ill adults with and without AKI, markers of bone and mineral metabolism (25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone, ionized and total serum calcium, phosphorus, bone specific alkaline phosphatase, osteocalcin, tartrate resistant acid phosphatase, β-crosslaps) were measured. FGF-23 was measured using a C-terminal FGF-23 ELISA (Immutopics, San Clemente).
Results: The mean age was 63±16 years and 76% were men. FGF-23 levels were significantly higher in patients with AKI (median 2720 RU/ml, range 3518708) compared to patients without AKI (150 RU/ml, 5514 000; P<0.001) and nonsignificantly higher in nonsurvivors (n=12, 624 RU/ml, 618709) compared to survivors (312 RU/ml, 5514 000, P=0.453). There was no significant correlation between FGF-23 and any of the measured biochemical markers.
Discussion: In our small cohort of medical critically ill patients, FGF-23 levels were substantially higher than in other reported populations. In patients with AKI these were significantly higher than in patients without AKI. There was no significant correlation of FGF-23 and any of the determined markers of bone and mineral metabolism, although this may primarily be a matter of small sample size, as the correlation coefficient was strongest for serum phosphorus, ionized calcium and osteocalcin and reached values of almost 0.3. In conclusion, the role of FGF-23 in critical illness remains unclear and further studies on this topic are warranted.
17 May 2014 - 20 May 2014