Mitigating peritoneal membrane characteristics in modern peritoneal dialysis therapy
- PMID: 17080116
- DOI: 10.1038/sj.ki.5001920
Mitigating peritoneal membrane characteristics in modern peritoneal dialysis therapy
Abstract
Membrane function at the start of peritoneal dialysis (PD) treatment, measured as solute transport rate and ultrafiltration capacity, varies considerably between individuals. Although this can be correlated to clinical factors such as age and body habitus, this accounts for little of the variance seen. It is increasingly clear, however, that this variability in membrane function does impact on clinical outcomes. Specifically, high solute transport increases mortality risk, independent of other known factors such as age, comorbidity, and residual renal function. High solute transport causes earlier loss of the osmotic gradient when a low molecular weight osmolyte such as glucose is used. This will result in an earlier and lower peak in the ultrafiltration achieved combined with a higher fluid absorption rate once the osmotic gradient is lost. It is therefore quite plausible that the worse clinical outcomes associated with high transport reflect less good ultrafiltration, although other explanations must be considered, including higher peritoneal protein losses and a possible association with systemic inflammation. Strategies now exist to mitigate the effects of high transport on fluid removal. These include optimization of the short dwell lengths using automated PD (APD) combined with icodextrin which will result in sustained ultrafiltration and thus prevention of reabsorption in the long dwell. Survival analysis of APD patients, especially in cohorts in which icodextrin has been used, would suggest that high transport status is not a risk factor, although some of these data are only preliminary. In contrast, low ultrafiltration capacity of the membrane seems to be more important in these patients, especially if anuric. Here the best strategy would seem to be prevention as patients who develop low ultrafiltration capacity are not easily treated on PD. Avoiding excessive hypertonic glucose exposure and preserving residual renal function offers the best available approach.
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