Vitamin D has anti-inflammatory properties, and deficiency is prevalent in children. There is a paucity of data regarding vitamin D status and its correlation with low-grade inflammation and vasculature. We prospectively enrolled 25 children, 9–11 years old (13 male); 21 obese. Eight atherosclerosis-promoting risk factors were scored as categorical variables with the following thresholds defining abnormality: body mass index Z score ≥1.5; systolic blood pressure ≥95th percentile (for age, sex, and height); triglyceride ≥100 mg/dL; low-density lipoprotein cholesterol (LDL-C) ≥110 mg/dL; high-density lipoprotein cholesterol ≤45 mg/dL; hemoglobin A1C (HBA1C) ≥5.5; 25-hydroxyvitamin D [25(OH) D] ≤30 ng/mL, and tobacco smoke exposure. High-sensitivity C-reactive protein (hsCRP) was measured to assess low-grade inflammation and classified as low- (<1 mg/L), average- (1–3 mg/L), and high-risk (>3 to <10 mg/L) groups. The proportion of children within each hsCRP group who had above threshold risk factors was calculated. Carotid artery ultrasound was performed to measure carotid artery intima-media  thickness (CIMT). Median (range) for 25(OH) D was 24 (17–45) ng/mL. Eighteen were either 25 (OH) D deficient (<20 ng/mL) or insufficient (20–30 ng/mL), and seven were sufficient (>30 ng/mL). hsCRP was 1.7 (0.2–9.1) mg/L, with 11 being <1.0 mg/L, 8 between 1.0–3.0 and 6 > 3.0 to < 10.0 mg/L. Risk factor score was 3.9 ± 1.7 out of eight. 25(OH) D levels did not correlate with hsCRP or CIMT. While vitamin D deficiency, inflammation, and risk factors coexist at a very young age, causative mechanisms remain unclear.