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Background and Aims: Icodextrin is a starch-derived glucose polymer that causes sustained ultrafiltration in long dwells in peritoneal dialysis. The aim of this study was to assess factors that were predictive of an increment in ultrafiltration following the introduction of icodextrin in patients with refractory fluid overload., Methods: Thirty-nine patients (20 male/19 female, mean age 57.7 +/- 2.4 years) on peritoneal dialysis were enrolled in a prospective pretest/post-test, open-label study. All patients had symptomatic fluid overload refractory to fluid restriction (<800 mL/day), frusemide doses of 250 mg or more daily, optimization of dwell time and use of hypertonic dextrose. An icodextrin exchange was substituted for a 4.25% dextrose exchange for the long-dwell period., Results: After 1 month, median (interquartile range) 24 h ultrafiltration volume increased by 500 mL (interquartile range: 50-1000). An increase in ultrafiltration volume correlated positively with the dialyate : plasma creatinine ratio at 4 h (r = 0.498, P = 0.001) and negatively with the ratio of dialysate glucose concentrations at 4 and 0 h (r = -0.464, P = 0.003). On multivariate regression analysis, high transporter status was predictive of a greater ultrafiltration response to icodextrin relative to dextrose peritoneal dialysis exchanges. Age, sex, race, peritoneal dialysis duration, peritoneal dialysis modality, diabetes mellitus, baseline albumin, and baseline ultrafiltration volume were not significantly correlated with the change in ultrafiltration volume., Conclusion: Icodextrin significantly augments ultrafiltration volumes in patients with refractory fluid overload. A high peritoneal membrane transporter status is the best predictor of a favourable ultrafiltration response to icodextrin.

Previous retrospective studies have reported that icodextrin may prolong peritoneal dialysis (PD) treatment time in patients with refractory fluid overload (RFO). Because the annual cost of PD therapy is lower than that of hemodialysis (HD) therapy in Australia, we prospectively investigated the ability of icodextrin to prolong PD technique survival in patients with RFO. We used a computer model to estimate the savings associated with that therapeutic strategy, based on annual therapy costs determined in a regional PD and HD costing exercise. Patients who met standard criteria for RFO and who were otherwise to be converted immediately to HD, were asked to consent to an open-label assessment of the ability of icodextrin to delay the need to start HD. Time to conversion to HD was measured. The study enrolled 39 patients who were followed for a mean period of 1.1 years. Icodextrin significantly increased peritoneal ultrafiltration by a median value of 368 mL daily. It prolonged technique survival by a mean period of 1.21 years [95% confidence interval (CI): 0.80-1.62 years]. Extension of PD treatment time by icodextrin was particularly marked for patients who had ultrafiltration failure (UFF, n = 20), defined as net daily peritoneal ultrafiltration < 1 L daily (mean extension time: 1.70 years; 95% CI: 1.16-2.25 years). Overall, annualized savings were US$3,683 per patient per year. If just the patients with UFF were considered, the savings increased to US$4,893 per year. Icodextrin prolongs PD technique survival in patients with RFO, permitting them to continue on their preferred therapy. In Australia, that practice is highly cost-effective, particularly in individuals with UFF.