Many physicians estimate hydration status by using clinical parameters, such as edema, weight gain or blood pressure. Although there was a direct correlation between systolic blood pressure and tissue hydration, a substantial proportion of patients did not comply with this paradigm. A number of patients had systolic hypertension, despite normohydration or even tissue underhydration. These are probably patients who suffer from vascular stiffness. Further dehydration of these patients in an attempt to normalize blood pressure might be dangerous, as it might abruptly compromise coronary perfusion. A number of patients had a low or normal blood pressure, despite being fluid overloaded. It is conceivable that many of these patients suffer congestive heart failure. Normotension in these patients NVP-BKM120 distributor should not be seen as equivalent to euvolemia, as also reported in HD patients. In many studies on fluid overload, attention is focused on fluid output, neglecting that fluid status is a balance of fluid output and input. In the EuroBCM study, there was a very weak association between fluid overload and diuresis, but this association disappeared in the multivariate analysis. Davison et al found a small influence of residual GFR, but not of peritoneal ultrafiltration or daily urine output, on volume status. Wiggins et al demonstrated that total fluid output one month after the initiation of PD was not associated with patient survival. All these point out that in studies on fluid status, both fluid input and output should be considered. In addition, and maybe even more of importance, clinicians should be aware that patients can be overhydrated because of dietary incompliance, despite having substantial residual diuresis. Dietary intake of fluid and salt should thus be conisdered when managing fluid overloaded patients. In our BCM cohort, the use of high hypertonic bags was associated with fluid overload. It is tempting to attribute this observation to bias by indication. However, an alternative potential hypothesis could be that the strategy of using hypertonic bags is not effective in returning patients back to euvolemia for a sustained period of time, as it can lead to dysregulation of glycemic control, and thus to hyperosmolarity and thirst. Sustained exposure to hypertonic exchanges can also negatively impact on the peritoneal membrane function, leading to further detrimental consequences on fluid balance. Further studies in this regard are warranted. This is compatible with the negative impact of high initial peritoneal fluid removal : it is likely that those with a high fluid output achieved this at the expense of increased use of hypertonic bags, thus damaging the peritoneal membrane in the long term. There was an association between peritoneal membrane transport characteristics and tissue hydration, as already demonstrated by others.