['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.', '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 [iPTH], 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.', '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 μg/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.'] Are fibroblast growth factor 23 and fetuin A independent predictors for the coronary artery disease extent in mild chronic kidney disease?