DOES IMPAIRED TRANSCELLULAR WATER TRANSPORT CONTRIBUTE TO NET ULTRAFILTRATION FAILURE DURING CAPD

Objectives: To assess the contribution of transcellular water transpor t in net ultrafiltration failure during continuous ambulatory peritone al dialysis (CAPD). Design: Retrospective. Setting: Renal Unit, Academ ic Medical Center, Amsterdam. Patients: One group of 6 patients with c linical severe ultrafiltration loss and a group of 10 stable CAPD pati ents without ultrafiltration problems. Intervention: In all patients, two peritoneal permeability tests were done within one week, using glu cose 1.36% dialysate on one day and glucose 3.86% on the other day. De xtran 70 was used as a volume marker. Results: The difference in net u ltrafiltration between 3.86% glucose and 1.36% glucose dialysate was 5 69+/-51 ml (control) and 153+/-103 mL (poor ultrafiltration group; p < 0.005). The dialysate/plasma (D/P) concentration ratios increased in both groups with glucose 1.36%. When using 3.86% glucose, the D/P rati o decreased in the control group with a median minimum value one hour after completion of inflow. It is possible that sieving of sodium was due to transcellular water transport by crystalloid osmosis during the hypertonic dwell, as a dissociation between the transport of water an d sodium is unlikely to occur in transport through the much larger int ercellular pores. The D/P sodium ratio after one hour was related to t he mass transfer area coefficient (MTC) of creatinine and the percenta ge of glucose absorption in the control group. No decrease in D/P rati o was found in the poor ultrafiltration group. This suggests impairmen t of transcellular water transport. No significant differences were pr esent between both groups with regard to MTC creatinine (10.2 and 14.0 mL/min), glucose absorption (71% and 71%), effective lymphatic absorp tion rate (1.34 and 1.01 mL/min), and residual volume(248 and 178 mL). Only 1 patient in the ultrafiltration loss group continued with CAPD. The others had to be transferred to hemodialysis; 1 of them developed sclerosing peritonitis. Conclusion: The sieving of sodium during CAPD may be caused by transcellular water transport. Deficient sieving as assessed by the absence of a decreased D/P ratio after one hour of a h ypertonic dwell suggests impairment of transcellular water transport. This is associated with severe ultrafiltration failure. It indicates t hat failure of transcellular water transport, possibly by glycosylatio n of specific proteins on the cell membrane, may be considered one of the causes of ultrafiltration failure during CAPD.