Background: It has recently been found that both estrogens and testosterone may inhibit vascular calcification but the role of sex hormones in the development of cardiovascular complications in chronic kidney disease (CKD) is still unclear. Aim of the study: The aim of the study was to assess the relations between sex hormones, coronary artery calcification (CAC) and atherosclerosis in postmenopausal women with CKD stage 3-5. Material and methods: In a cross-sectional study, serum estradiol, testosterone, dehydroepiandrosterone sulfate (DHEA), 25-hydroxyvitamin 03 (25-OH-D3), mineral parameters and lipids were measured in 36 Caucasian, non-dialysed amenorrheic women (mean age 56.8 +/- 11.4 yrs), with CKD stage 3-5 (mean eGFR 20.8 +/- 8.8 ml/min/m(2)), without any history of major cardiovascular events. CAC was measured with multidetector computed tomography and common carotid artery intima media thickness (CCA-IMT) with ultrasound. Results: The prevalence of CAC (CAC score > 30 Agatston units) was 44.4%. Mean CAC score in women with detectable calcification was 177.3 +/- 268.4. The women who did not develop vascular calcification had also lower CCA-IMT (0.65 +/- 0.13 vs. 0.88 +/- 0.12 mm, p < 0.0004). In women with CAC, serum estradiol was significantly higher than in those without CAC (30.1 +/- 14.2 vs. 14.7 +/- 7.44 pg/mL, p < 0.001). Similarly, a testosterone level in women with CAC was higher than in those without CAC (5.4 +/- 4.2 vs. 2.3 +/- 1.3 pg/mL, p < 0.006) and the same was observed for DHEA-s (100.5 +/- 67.6 vs. 60.3 +/- 56.4 mu g/dL, respectively; p < 0.05). Serum 25-OH-D3 was similar in both groups. There was a significant correlation between the serum level of estradiol and CAC score (R = 0.533, p < 0.05) and between the serum estradiol level and total cholesterol (R = 0.505, p < 0.05), LDL-Ch (R = 0.585, p < 0.05), phosphorus level (R = 0.4, p < 0.03) and calcium-phosphorus index (Ca x P: R = 0.44, p < 0.04) and between serum testosterone and total cholesterol (R = 0.5, p < 0.05). Conclusion: Our results do not support the inhibitory effects of endogenous sex hormones on vascular calcification in postmenopausal women with advanced chronic kidney disease.