Abstract: TH-PO183
Adjustment for ProBNP Substantially Attenuates Prognostic Implications of Plasma FGF23 Levels in CKD
Session Information
- Bone and Mineral Metabolism: Clinical - I
October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 402 Bone and Mineral Metabolism: Clinical
Authors
- Emrich, Insa E., Saarland University Medical Center, Homburg (Saar), Germany
- Brandenburg, Vincent, Rhein-Maas Klinikum, Würselen, Germany
- Sellier, Alexander, Saarland University Medical Center, Homburg (Saar), Germany
- Seiler-Mussler, Sarah, Gemeinschaftspraxis Dr. Schürfeld, Dr. Möller, Dr. Henrich, Saarlouis, Germany
- Heine, Gunnar H., Saarland University Faculty of Medicine, Homburg, Germany
Background
Various epidemiological studies linked high plasma levels of the phosphatonin FGF23 with cardiovascular events in non-dialysis CKD. It remains enigmatic whether high FGF23 exerts adverse cardiovascular effects, or whether it reflects detrimental effects of residual confounders. Earlier epidemiological studies adjusted for chronic kidney disease – mineral bone disease (CKD-MBD) regulators of FGF23 rather than for recently discovered non-CKD-MBD regulators, among which iron deficiency and heart failure are of particular importance. Moreover, they used c-terminal FGF23 assays (cFGF23) rather than more specific intact FGF23 assays (iFGF23).
Methods
The CARE FOR HOMe study analyzed plasma ferritin, hepcidin, iFGF23, cFGF23 and proBNP along with conventional risk factors, among 575 CKD G2-G4 patients. The participants were followed 5.1 ± 2.1 years for the occurrence of atherosclerotic events and hospitalization for acute decompensated heart failure, respectively.
Results
cFGF23 correlated strongly with high iFGF23, fairly with high proBNP and weakly with low ferritin; correlation coefficients of iFGF23 with proBNP and ferritin were numerically lower. In Kaplan-Meier analyses, both endpoints were predicted by cFGF23 and iFGF23. In Cox regression models, cFGF23 remained an outcome predictor after adjustment for conventional risk factors and iron deficiency. This prediction was largely eliminated when further adjusting for proBNP. iFGF23 was less consistently associated with adverse outcome in partly adjusted models, and failed to predict outcome in fully adjusted models.
Conclusion
In summary, iron deficiency and heart failure affect plasma FGF23. As adjustment for proBNP virtually eliminates the prognostic implications of plasma FGF23, we speculate that high FGF23, rather than exerting detrimental cardiovascular effects, merely mirrors prevalent heart disease.