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Fibroblast Growth Factor 23 (FGF23) Predicts Progression of Chronic Kidney Disease: The Mild to Moderate Kidney Disease (MMKD) Study

Danilo Fliser^*, Barbara Kollerits, Ulrich Neyer, Donna P. Ankerst^,, Karl Lhotta^||, Arno Lingenhel, Eberhard Ritz^¶, Florian Kronenberg for the MMKD Study Group

^* Department of Internal Medicine, Hannover Medical School, Hannover, Germany; Division of Genetic Epidemiology; Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Innsbruck, Austria; Department of Nephrology and Dialysis, Academic Teaching Hospital, Feldkirch, Austria; Department of Urology, University of Texas Health Science Center at San Antonio, San Antonio, Texas; ^|| Department of Clinical Nephrology, Innsbruck University Hospital, Innsbruck, Austria; and ^¶ Department of Internal Medicine, Division of Nephrology, Ruperto-Carola-University, Heidelberg, Germany

Correspondence: Dr. Danilo Fliser, Department of Internal Medicine, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. Phone: +49-511-532-6319; Fax: +49-511-552366; E-mail: fliser.danilo{at}mh-hannover.de

Received for publication August 29, 2006. Accepted for publication May 22, 2007.

It has not been firmly established whether disturbed calcium-phosphate metabolism affects progression of chronic kidney disease (CKD) in humans. In this cohort study of 227 nondiabetic patients with CKD, we assessed fibroblast growth factor 23 (FGF23) plasma concentrations in addition to other variables involved in calcium-phosphate metabolism, and we followed 177 of the patients prospectively for a median of 53 months to assess progression of renal disease. In the baseline cohort, we found a significant inverse correlation between glomerular filtration rate and both c-terminal and intact FGF23 levels (both P < 0.001). The 65 patients who experienced a doubling of serum creatinine and/or terminal renal failure were significantly older, had a significantly lower glomerular filtration rate at baseline, and significantly higher levels of intact parathormone, c-terminal and intact FGF23, and serum phosphate (all P < 0.001). Cox regression analysis revealed that both c-terminal and intact FGF23 independently predict progression of CKD after adjustment for age, gender, GFR, proteinuria, and serum levels of calcium, phosphate, and parathyroid hormone. The mean follow-up time to a progression end point was 46.9 (95% CI 40.2 to 53.6) months versus 72.5 (95% CI 67.7 to 77.3) months for patients with c-terminal FGF23 levels above or below the optimal cut-off level of 104 rU/mL (derived by receiver operator curve analysis), respectively. In conclusion, FGF23 is a novel independent predictor of progression of renal disease in patients with nondiabetic CKD. Its pathophysiological significance remains to be elucidated.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673