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      Volume Control in Peritoneal Dialysis Patients: Role of New Dialysis Solutions

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          Abstract

          This paper reviews the most recent clinical data on the volume status of long-term peritoneal dialysis (PD) patients. It appears that many PD patients are volume overloaded, associated with a high prevalence of hypertension and left ventricular hypertrophy. In the presence of the poor results in patients with peritoneal ultrafiltration, the introduction of the polyglucose solution, icodextrin, has ameliorated volume control in some of these patients. In a second part of the review, some of the structural and functional alterations in the peritoneal membrane and the role of glucose degradation products (GDP) in the commonly used dialysates as well as the resulting formation of advanced glycation end products are described. The introduction of low GDP-containing solutions at normal pH has at least in experimental models of PD attenuated the hemodynamic changes observed with the classical solutions. The solutions at normal pH containing either bicarbonate or a mixture of bicarbonate/lactate were clinically associated with less inflow pain.

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          Most cited references 12

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          Effect of fluid and sodium removal on mortality in peritoneal dialysis patients.

          Effect of fluid and sodium removal on mortality in peritoneal dialysis patients. Adequacy of peritoneal dialysis (PD) traditionally is assessed using Kt/V(urea) and total creatinine clearance (TCC). However, this approach underestimates the importance of fluid and sodium removal. The aim of this study was to determine the effect of fluid and sodium removal on morbidity and mortality in PD patients. One hundred twenty-five PD patients were monitored for three years from the beginning of the treatment. The effects of demographic features, comorbidity, peritonitis rate, blood pressure, medications, blood biochemistry, peritoneal membrane transport characteristics, residual renal function (RRF), Kt/V(urea), TCC, normalized protein nitrogen appearance (nPNA), and removal of sodium and fluid on mortality were evaluated. Total and cardiovascular hospitalization rates were also recorded. A Cox proportional hazards model was used to determine factors predicting mortality. In the Cox model, comorbidity, total sodium and fluid removals, hypertensive status, serum creatinine, and RRF were independent factors affecting survival. In contrast, Kt/V(urea) or TCC did not affect the adjusted survivals. Total sodium and fluid removal and hypertensive status also significantly influenced the hospitalization rate. Systolic and diastolic blood pressures were negatively correlated with total fluid (P < 0.001) and sodium removal (P < 0.001). Together, these findings suggest that removal of sodium and fluid is a predictor of mortality in PD patients, whereas Kt/V(urea) and TCC are not factors. Adequate fluid and sodium balance is crucial for the management of patients on PD.
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            Long-term clinical effects of a peritoneal dialysis fluid with less glucose degradation products.

            Glucose degradation products (GDPs) are cytotoxic in vitro and potentially toxic in vivo during peritoneal dialysis (PD). We are presenting the results of a two-year randomized clinical trial of a new PD fluid, produced in a two-compartment bag and designed to minimize heat-induced glucose degradation while producing a near neutral pH. The effects of the new fluid over two years of treatment on membrane transport characteristics, ultrafiltration (UF) capacity, and effluent markers of peritoneal membrane integrity were investigated and compared with those obtained during treatment with a standard solution. A two-group parallel design with 80 continuous ambulatory peritoneal dialysis patients was used. The patients were randomly assigned to either the new fluid (N = 40) or to a conventional one (N = 40), and were stratified with respect to age, diabetes, and time on PD. Peritoneal transport characteristics were assessed by the Personal Dialysis Capacity (PDCtrade mark) test at 1, 6, 12, 18, and 24 months after inclusion and by weighing the overnight bag daily. Infusion pain and handling were evaluated using a questionnaire. Peritoneal mesothelial and interstitial integrity were evaluated by analyzing overnight effluent dialysate concentrations of CA 125, hyaluronan (HA), procollagen-1-C-terminal peptide (PICP), and procollagen-3-N-terminal peptide (PIIINP) at 1, 6, 12, 18, and 24 months. The handling of the new two-compartment bag was considered easy, and there were no indications of increased discomfort with the new system. Furthermore, no changes in peritoneal fluid or solute transport characteristics were observed during the study period for either fluid, and neither were there any differences with regard to peritonitis incidence. However, significantly higher dialysate CA 125 (73 +/- 41 vs. 25 +/- 18 U/mL), PICP (387 +/- 163 vs. 244 +/- 81 ng/mL), and PIIINP (50 +/- 24 vs. 29 +/- 13 ng/mL) and significantly lower concentrations of HA (395 +/- 185 vs. 530 +/- 298 ng/mL) were observed in the overnight effluent during treatment with the new fluid. We conclude that the new fluid with a higher pH and less GDPs is safe and easy to use and has no negative effects on either the frequency of peritonitis or peritoneal transport characteristics as compared with conventional ones. Our results indicate that the new solution causes less mesothelial and interstitial damage than conventional ones; that is, it may be considered more biocompatible than a number of conventional PD solutions currently in use.
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              AGEs bind to mesothelial cells via RAGE and stimulate VCAM-1 expression.

              Excess advanced glycation end-products (AGEs) are formed during renal failure, and AGE formation also may be connected with the high glucose concentration of peritoneal dialysis (PD) fluids. To determine the effect of human peritoneal mesothelial cell (HPMC) exposure to glycated proteins, we studied the HPMC receptor of AGE expression (RAGE), and analyzed the results of AGE-RAGE interaction on adhesion molecule expression and leukocyte binding. RAGE was detected by FACS analysis, and RAGE mRNA by reverse transcription-polymerase chain reaction (RT-PCR). Vascular and intercellular cell adhesion molecule (VCAM-1 and ICAM-1) expression was measured by a known radiometric technique under basal conditions, after the addition of an AGE-specific compound, Nepsilon-carboxylmethyllysine (CML-albumin). Leukocyte adhesion on HPMC was analyzed by videomicroscopy after HPMC stimulation. RAGE protein was detected on HPMC, and RAGE mRNA was evidenced by RT-PCR. VCAM-1 expression was stimulated by CML-albumin (P < 0.01), while ICAM-1 was unchanged. By blocking the AGE-RAGE interaction, anti-RAGE antibodies or recombinant RAGE inhibited the increase in VCAM-1 expression. CML-albumin stimulation potentiated leukocyte adhesion to HPMC (P < 0.001). This effect was prevented by the incubation of leukocytes with recombinant VCAM-1 (P < 0.001). AGE binding to RAGE stimulated mesothelial cell activity, and resulted in the overexpression of VCAM-1, a structure for leukocyte adhesion. The AGE-RAGE interaction resulted in HPMC activation, which may promote local inflammation, and thus is implicated in the peritoneal injury found in long-term PD patients.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                978-3-8055-7683-3
                978-3-318-01049-7
                0253-5068
                1421-9735
                2004
                July 2004
                20 January 2004
                : 22
                : 1
                : 44-54
                Affiliations
                Renal Division, University Hospital, Ghent, Belgium
                Article
                74923 Blood Purif 2004;22:44–54
                10.1159/000074923
                14732811
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                References: 109, Pages: 11
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/74923
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