Use of routine measurements in an unselected population also means that these results are likely to be generalizable across the 
United Ganoderic-acid-G Kingdom and in other countries with similar dialysis schedules and patient populations. In addition, there is potential for selection bias in our 20(S)-Notoginsenoside-R2 findings as follow up was censored when patients received a kidney transplant or transferred to peritoneal dialysis. These people are likely to be healthier, and may have lower BP variability. However, this represents less than 15% of the initial cohort and there was no other loss-to follow-up. Finally, we were not able to examine cause-specific mortality which might have provided greater etiological insight. Mortality in haemodialysis patients is markedly higher than in the general population and cardiovascular disease is the main cause of death. Conventional measures of BP are linearly associated with cardiovascular risk in the general population. However, among patients undergoing haemodialysis, many studies demonstrate a non-linear relationship between mean BP and mortality. In this group there is increasing evidence that BP variability may be more closely associated with adverse outcomes than conventional measures of BP. Patients with ESRD have greater visit to visit BP variability compared to the general population. Tozawa et al showed that systolic BP variability, quantified by coefficient of variation, predicted all-cause but not cardiovascular mortality in a cohort of 144 Japanese dialysis patients. However, this study was limited by a small number of deaths during the study period. A further study by Rossignol and colleagues examined the role of BP variability in a cohort of 397 haemodialysis patients with left ventricular hypertrophy enrolled in an interventional study. They showed that visit-to-visit systolic and diastolic BP variability was associated with a composite end-point of cardiovascular events during follow-up while baseline SBP and DBP were not. A recent study by Chang et al in a cohort of 1844 haemodialysis patients from the HEMO study showed that visit-to-visit SBP variability, quantified by coefficient of variation and average real variability, predicted all-cause and cardiovascular mortality. All three of these studies were limited by inclusion of prevalent haemodialysis patients. Only one study has demonstrated an association between pre-dialysis systolic and diastolic BP variability and all-cause mortality in an incident dialysis cohort. However this study was limited by an extremely short-follow-up meaning that reverse causality was a strong potential explanation of their findings. BP variability during haemodialysis has also been associated with all-cause and cardiovascular mortality, as has changing pre-dialysis systolic and diastolic BP over time. While examining slightly different hypotheses, it is likely that they reflect similar underlying pathophysiology to studies of pre-dialysis systolic BP variability. The mechanisms that contribute to increased BP variability in patients with ESRD are complex and poorly understood. They include changes in intravascular volume and vasoactive factors, reduced arterial compliance, increased sympathetic innervation and alterations of arterial and cardiopulmonary reflexes. Poor or variable compliance with fluid restriction and antihypertensive therapy could also contribute to BP fluctuations. Whether increased BP variability is causal in cardiovascular events and mortality, or whether it is a marker of vascular disease and autonomic dysfunction, is still subject to debate. Strong arguments have been made for changes in BP as a direct mechanism of event causation in cohorts without CKD.