• David E Leaf, Marta Christov, Harald Jüppner, Edward Siew, T Alp Ikizler, Aihua Bian, Guanhua Chen, Venkata S Sabbisetti, Joseph V Bonventre, Xuan Cai, Myles Wolf, and Sushrut S Waikar.
• Division of Renal Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. Electronic address: deleaf@partners.org.
• Kidney Int. 2016 Apr 1; 89 (4): 939-48.

AbstractFibroblast growth factor 23 (FGF23) is elevated in chronic kidney disease and associated with increased mortality, but data on FGF23 in humans with acute kidney injury (AKI) are limited. Here we tested whether FGF23 levels rise early in the course of AKI following cardiac surgery and if higher postoperative FGF23 levels are independently associated with severe AKI and adverse outcomes. Plasma C-terminal FGF23 (cFGF23) levels were measured preoperatively, at the end of cardiopulmonary bypass, and on postoperative days 1 and 3 in 250 patients undergoing cardiac surgery. We also measured intact FGF23, parathyroid hormone, phosphate, and vitamin D metabolites in a subgroup of 18 patients with severe AKI and 18 matched non-AKI controls. Beginning at the end of cardiopulmonary bypass, cFGF23 levels were significantly and consistently higher in patients who developed AKI compared with those who did not. The early increase in cFGF23 predated changes in other mineral metabolites. The levels of intact FGF23 also increased in patients who developed severe AKI, but the magnitude was lower than cFGF23. In analyses adjusted for age, preoperative eGFR, and cardiopulmonary bypass time, higher cFGF23 levels at the end of cardiopulmonary bypass were significantly associated with greater risk of severe AKI and the need for renal replacement therapy or death. Thus, cFGF23 levels rise early in AKI following cardiac surgery and are independently associated with adverse postoperative outcomes. Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

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