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  • Title: Does impaired transcellular water transport contribute to net ultrafiltration failure during CAPD?
    Author: Monquil MC, Imholz AL, Struijk DG, Krediet RT.
    Journal: Perit Dial Int; 1995; 15(1):42-8. PubMed ID: 7734560.
    Abstract:
    OBJECTIVES: To assess the contribution of transcellular water transport in net ultrafiltration failure during continuous ambulatory peritoneal dialysis (CAPD). DESIGN: Retrospective. SETTING: Renal Unit, Academic Medical Center, Amsterdam. PATIENTS: One group of 6 patients with clinical severe ultrafiltration loss and a group of 10 stable CAPD patients without ultrafiltration problems. INTERVENTION: In all patients, two peritoneal permeability tests were done within one week, using glucose 1.36% dialysate on one day and glucose 3.86% on the other day. Dextran 70 was used as a volume marker. RESULTS: The difference in net ultrafiltration between 3.86% glucose and 1.36% glucose dialysate was 569 +/- 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 ratio 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 and sodium is unlikely to occur in transport through the much larger intercellular pores. The D/P sodium ratio after one hour was related to the mass transfer area coefficient (MTC) of creatinine and the percentage of glucose absorption in the control group. No decrease in D/P ratio was found in the poor ultrafiltration group. This suggests impairment of transcellular water transport. No significant differences were present between both groups with regard to MTC creatinine (10.2 and 14.0 mL/min), glucose absorption (71% and 71%), effective lymphatic absorption 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 hypertonic dwell suggests impairment of transcellular water transport. This is associated with severe ultrafiltration failure. It indicates that failure of transcellular water transport, possibly by glycosylation of specific proteins on the cell membrane, may be considered one of the causes of ultrafiltration failure during CAPD.
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