Residual renal function, peritoneal transport characteristics and dialysis adequacy in peritoneal dialysis.
For patients treated with standard CAPD the residual renal function has a major effect for the ability to achieve target Kt/Vurea and nKCr, whereas the impact of peritoneal transport characteristics is negligible for urea and still rather small for creatinine compared to the impact of the residual renal function. However, when the dialysis prescription is adjusted as residual renal function declines with time on CAPD, the peritoneal transport characteristics markedly influence the increase in creatinine clearance with increased dialysate volume. There are several practical factors that also may limit the possibility of achieving target Kt/Vurea and nKCr among peritoneal dialysis patients with minimal residual renal function. There are limits to the number of exchanges and to the dwell volume a patient will accept and increased dwell volumes may also increase fluid absorption due to increased intraperitoneal hydrostatic pressure. Furthermore, for APD, dialysate flow rates may limit the treatment efficacy if the catheter function is poor. If dialysate flow rate in APD is high, the diffusive transport capacity of the peritoneal membrane may be the limiting factor for dialysis efficacy (in addition to treatment time). Therefore, it is important to monitor peritoneal diffusive transport characteristics, such as by the PET, before any large change in dialysis prescription is made. Patient and technique survival are better among CAPD patients with a higher level of residual renal function and also seem to be related to the peritoneal transport characteristics per se, as patients with high transport rates seem to have worse clinical outcomes. It is possible that these effects may be related to the increased peritoneal losses of nutrients in patients with high peritoneal transport rates or to the less efficient fluid removal among patients with low residual renal function and high peritoneal transport rates.
Heimbürger
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Department of Clinical Sciences, Karolinska Institute, Huddinge University Hospital, Sweden.
D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000503:physiopathology* / Q000628:therapy*; D010529:Peritoneal Cavity / Q000502:physiology*; D010530:Peritoneal Dialysis; D016896:Treatment Outcome