Furthermore, when smokers were dichotomized by the median value of the amount of smoking, the proportion of patients with AoAC at baseline was significantly higher in heavy smokers compared to light smoker group. Based on these findings, it was presumed that not only the smoking status but also the amount of smoking could affect the risk of AoAC. However, due to limited information about detailed smoking status, the relationship of the smoking status and the amount of smoking with AoAC could not be thoroughly clarified in this study. Compared to Paclitaxel Microtubule inhibitor previous studies on the association of various parameters with vascular calcification and the clinical consequences of vascular calcification, the risk factors for the progression of vascular calcification are largely unexplored in dialysis patients. In addition, impacts of the vascular calcification progression on these patients’ outcome have not been elucidated. A previous study by Sigrist et al investigated the independent factors associated with the progression of vascular calcification and the influence of it on mortality over 24 months in 134 patients with stage 4 and 5 CKD. It found that progressive calcification was associated with age, male gender, and serum alkaline phosphatase levels. Similarly, the NECOSAD study showed that age, hypercalcemia, hyperparathyroidism, and the interval between the first and last assessed AoACS were significantly linked with an increase in calcification score over time. Kim et al also found that age, dialysis duration, and the presence of AoAC were related to AoAC progression. However, in those studies, about two-thirds of patients were HD patients. In addition, changes in calcification score were significantly higher in HD patients than in PD patients. Moreover, the interval between the first and last measurement of AoACS was inconsistent in the NECOSAD study. In this study, only incident PD patients were included and the interval between the first and follow-up AoACS assessment was 12 months in all patients. Therefore, the results of the aforementioned studies may not be applicable to ours. Even though age was significantly associated with AoAC progression in our subjects, when analysis was preformed separately according to the baseline AoAC presence, the association of age and AoACS with progression remained meaningful only in patients without baseline AoAC. Considering that age was significantly higher in patients with baseline AoAC than in patients without, we surmised that the effect of age on AoAC progression might be lessened in elderly incident PD patients who already had AoAC. In the present study, AoAC progression was an independent predictor of unfavorable outcome in incident PD patients, which is in agreement with the results of most previous studies. However, the mechanism by which AoAC progression influences mortality in ESRD patients has not been fully understood. We suppose that a different type of vascular calcification can be one of the possible mechanisms. London et al examined the impact of intimal and medial calcification on the prognosis in prevalent HD patients and found that arterial medial calcification was a much stronger predictor of mortality than arterial intimal calcification in these patients. On the other hand, it is well known that chronic inflammation, malnutrition, and atherosclerosis are closely linked with each other in ESRD patients. Furthermore, the current study demonstrated that AoAC progression was observed even in patients without baseline AoAC and that AoAC progression was significantly associated with elevated hs-CRP levels in both baseline AoAC present and absent groups. Based on these findings, we surmised that AoAC progression was associated with AMC progression specific to dialysis therapy.