Fibroblast growth factor 23 and fetuin A are independent predictors for the coronary artery disease extent in mild chronic kidney disease.

Background and objectives: Cardiovascular disease in chronic kidney disease (CKD) is explained in part by traditional cardiovascular risk factors; by uremia-specific factors; and by abnormalities of mineral metabolism, factors involved in its regulation, and in the vascular calcification process. Design, setting, participants, & measurements: In an unselected population of 177 patients with calculated GFR (eGFR) between 90 and 30 ml/min per 1.73 m(2), the link between the mineral metabolism abnormalities (calcium, phosphorus, calcium-phosphorus product), regulatory factors (parathyroid hormone [PTH], intact PTH vitamin D, fibroblast growth factor 23 [FGF 23], and fetuin A), and the severity of coronary artery disease (CAD) assessed by coronary angiography were evaluated in three subgroups defined by tertiles of Gensini lesion severity score. Results: The mean serum values for FGF 23 in the entire study population was 28.1 +/- 17.3 RU/ml and for fetuin A was 473.1 +/- 156.2 mu g/ml. Patients with eGFR < 60 ml/min per 1.73 m(2) had significantly higher values of FGF 23 compared with patients with eGFR > 60 ml/min per 1.73 m(2). The Gensini score values significantly correlated with gender; arterial hypertension; and HDL cholesterol, eGFR, iPTH, FGF 23, and fetuin A levels. After the adjustments for traditional and uremia-related cardiovascular risk factors, the FGF 23 and fetuin A remained significant predictors of the Gensini score. Conclusions: This study suggests that in a relatively young population with mild-to-moderate alteration of kidney function and with less traditional cardiovascular risk factors, anomalies of the serum FGF 23 and fetuin A levels appear early in the course of disease and are independent major predictors for extent of CAD. Clin J Am Soc Nephrol 5: 1780-1786, 2010. doi: 10.2215/CJN.02560310