Cardiovascular mortality increases with progressive decline in kidney function. Oxidative stress is a risk factor for cardiovascular complications in patients with chronic kidney disease (CKD). Oxidative stress also increases as renal function declines. Dysfunctional mitochondria are a main source of oxidative stress and may contribute to the pathogenesis of cardiovascular disease in patients with CKD. In this study we tested the hypothesis that mitochondrial function decreases with the progression of CKD by assessing mitochondrial DNA (mtDNA) copy number from blood mononuclear cells (PBMCs) and plasma isofurans. Isofurans formation is favored over F2-Isoprostanes when oxygen tissue tension is high, as observed in mitochondrial dysfunction. Eighty three subjects were separated in 3 groups based on eGFR: CKD stage 1-2, CKD stage 3-4, and CKD stage 5 (hemodialysis). Groups were comparable in age, gender, BMI and prevalence of hypertension. Estimated marginal mean (after controlling for BMI) of mtDNA copy number in patients with CKD stage 5 was 1.72 (95% CI 0.10-3.34), lower than in patients with CKD stage 3-4 (3.44, 95% CI 0.98-5.90, p=0.02) and CKD stage 1-2 (6.56, 95% CI 4.57-8.54, p=0.008). F2-Isoprostanes were not different among CKD groups, whereas isofurans were higher in patients with CKD stage 5 (median 59.72; IQR 43.13-91.03) compared to CKD stages 3-4 (median 48.41; IQR 30.93-66.19, p=0.01), and CKD stage 1-2 (median 39.00; IQR 26.22-67.03, p=0.005). These results suggest that progressive kidney disease is associated with mitochondrial dysfunction. Further studies are required to evaluate in vivo mitochondrial function in patients with different CKD stages.