Successful long-term peritoneal dialysis (PD) requires preservation of the transport function of the peritoneal membrane. Adequate dialysis is not only a matter of achieving the targets for Kt/Vurea and creatinine clearance, but also—and maybe even more importantly—of maintaining an optimal volume status. The development of ultrafiltration failure (UFF) remains one of the most important causes of treatment drop-out. It is also associated with a poor prognosis. Evidence is mounting that the incidence of UFF increases with time spent on PD, suggesting that the peritoneal membrane is progressively damaged during PD. However, the nature and the causes of the structural and functional alterations of the peritoneal membrane in long-term PD remain to be fully defined. Undoubtedly, continuous exposure to unphysiologic dialysis solutions is an important pathogenetic element in this respect. In addition, the repeated acute inflammatory damage conferred by recurrent peritonitis episodes and the chronic low-grade inflammation associated with the uremic state are likely to contribute. The present article reviews the extant studies on the functional and structural alterations of the peritoneal membrane in long-term PD. In addition, it focuses on the evidence for dialysate bioincompatibility in the genesis of these changes. Finally, therapeutic strategies with the potential to preserve long-term peritoneal membrane function and structure are addressed.
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Vriese et al. (2001) studied this question.
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