2 patients. There are very little data in PD patients but the available evidence suggest that vascular and valvular calciﬁcation is an equally highly prevalent complication in the PD population. In two small surveys, at least 60% to 80% of the PD patients, were complicated with coronary artery calciﬁcation [15, 16]. The prevalence of cardiac valvular calciﬁcation ranges from 32% to 47% in PD patients [17, 18], in contrast to 19% to 84% in hemodialysis patients [19–24]. 3. Signiﬁcance of Vascular/Valvular Calciﬁcation in PD Patients In the general population, coronary artery calcium score provides a quantitative estimate of total atherosclerotic plaque burden and correlates with obstructive coronary artery disease [25]. In nondialysis chronic kidney disease (CKD) patients, similar association was observed between the severity of coronary artery calcium score and obstructive coronary artery disease [26]. Study in hemodialysis patients demonstrated a close relation between the severity of coronary artery calciﬁcation and prevalence of atheroscle- rotic vascular disease [10]. This is in keeping with recent similar analysis in PD patients showing that the severity of coronary artery calcium score was associated with the prevalence of atherosclerotic vascular disease (unpublished observation). On the other hand, the severity of coronary artery calcium score is predictive of arterial stiﬀening in patients with CKD [27] and is associated with increased risk of left ventricular hypertrophy [28]. Unlike in the general population, where calciﬁcation occurs mainly in the intimal layer and reﬂects atherosclerotic disease burden, vascular calciﬁcation in ESRD patients typically occurs both in the intimal and medial layer [29]. The medial calciﬁcation, known as Monckeberg’s medial calcinosis is also prominent in patients with diabetes. Medical calciﬁcation promotes arterial stiﬀening and is associated with increased risk of left ventricular hypertrophy and impaired coronary perfusion [30]. While both medial and intimal type of calciﬁcations predict mortality and cardiovascular death in ESRD patients, intimal calciﬁcation was associated with worse survival compared to medial calciﬁcation [14]. On the other hand, cardiac valvular calciﬁcation is a marker reﬂecting general- ized atherosclerosis and calciﬁcation in the PD patients [31]. 4. Clinical Course of Vascular/Valvular Calciﬁcation in Long-Term PD Patients Vascular calciﬁcation is a progressive and actively mediated disease. Goodman et al. showed in a cohort of young hemodialysis adults of rapid progression in coronary artery calciﬁcation over a mean follow-up period of 20 months [8]. In the subsequent study by Block et al., patients who had baseline coronary artery calciﬁcations showed signiﬁcant progression in coronary calciﬁcation while those without baseline calciﬁcation remained free from calciﬁcation during follow-up [32]. These data suggest that preexisting coronary artery calciﬁcation is one of the key factors predicting further progression of vascular calciﬁcation in ESRD patients. Our International Journal of Nephrology recent analysis also reported similar ﬁnding in PD patients (unpublished observation) in that PD patients without signiﬁcant baseline vascular calciﬁcation remained relatively free of calciﬁcation with time on dialysis. These data raised the possibility of some protective mechanisms or genetic factors in play that prevent patients from developing vascular calciﬁcation. 5. Contributing Factors to Vascular/Valvular Calciﬁcation in PD Patients The high incidence of vascular/valvular calciﬁcation in PD patients is contributed by both traditional and so- called nontraditional or kidney disease-related risk factors. Age is one of the major clinical factors associated with vascular/valvular calciﬁcation in dialysis patients [7, 10, 17, 33]. Some studies showed that the degree of coronary or valvular calciﬁcation increased with increasing duration of dialysis [7, 8, 17]. Disturbed mineral metabolism with resulting hyperphosphatemia has been suggested to play a major contributing role for vascular/valvular calciﬁcation in ESRD patients [8, 10, 12, 17]. According to a retrospective analysis from the USRDS, an elevated serum phosphorus or an elevated calcium × phosphorus product predicts all-cause mortality as well as cardiovascular mortality in hemodialysis patients [34]. Notably, patients with a high serum phosphorus ≥6.5 mg/dL was associated with an increased risk of death from coronary artery disease, sudden death, infection or other causes, compared with the low phosphorus group [34]. The Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD) study compared hemodialysis and PD patients and showed that hyper- phosphatemia with resulting high calcium ∗ phosphorus product had similar predictive value for mortality in PD and hemodialysis patients [35]. Having a serum phosphorus level >1.78 mmol/L was associated with a time-dependent adjusted hazard ratios of 1.6 and 1.4 for all-cause mortality in PD and hemodialysis patients, respectively. These data clearly indicated that optimizing phosphorus control is equally important in PD as in hemodialysis patients. In vitro study showed that inorganic phosphate induced an osteoblastic phenotypic change in vascular smooth muscle cells which led to the deposition of calcium and phosphate-containing apatite crystals [36]. This is in keeping with cross-sectional studies demonstrating an association between hyperphosphatemia and vascular calciﬁcation in ESRD patients [8, 10, 12, 33]. Hyperphosphatemia is also associated with an increased risk of valvular calciﬁcation in patients on PD [17]. Previous longitudinal study showed a signiﬁcant association between serum phosphorus and calcium × phosphorus product with changes in coronary artery calciﬁcation over 1 year in PD patients [37], providing further evidence to support the involvement of hyperphos- phatemia in vascular/valvular calciﬁcation in PD patients. As in hemodialysis patients, PD patients have a high prevalence of hyperphosphatemia. According to the NECOSAD study, around 40% of the long-term PD patients had serum phosphorus level above the Kidney Disease Outcome Quality Initiative (K/DOQI) target of 1.78 mmol/L