Background: Expression and/or excretion of fibroblast growth factor-23 (FGF23) and its co-receptor Klotho are\naltered in patients with end-stage renal disease. The possibility that the FGF23/?-Klotho system mediates the\naggravated cardiovascular outcome among patients with chronic kidney disease (CKD) has been suggested. We\ndetermined whether FGF23 and ?-Klotho concentrations are altered among patients with reduced renal function\nand proteinuria.\nMethods: Serum FGF23 and ?-Klotho were measured in cardiology patients who were not undergoing chronic\nhemodialysis. Estimated glomerular filtration rate (eGFR) was correlated negatively with FGF23 and positively with\n?-Klotho.\nResults: The correlation between FGF23 and the renal tubular maximum reabsorption rate of phosphate to the\nGFR (TmP/GFR) was not significant, but that between FGF23 and serum calcium or inorganic phosphate was\nsignificant among patients with an estimated GFR of less than 60 mL/min/m2. By stepwise multivariate regression\nanalysis, eGFR was selected as significant predictor for FGF23 or ?-Klotho among patients with an estimated GFR of\nless than 60 mL/min/m2; however, urine albumin/creatinine ratio was not selected as a predictor for FGF23 or\n?-Klotho irrespective of the eGFR levels. In patients with eGFR of <60 mL/min/1.73 m2, UACR was significantly\nassociated with log(FGF23); but, this association did not remain statistically significant in a multivariate model.\nConclusions: Among cardiology patients with various stages of CKD, serum concentrations of FGF23 and ?-Klotho\nwere associated with renal function, but not with the extent of proteinuria.
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