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      No increase in small-solute transport in peritoneal dialysis patients treated without hypertonic glucose for fifty-four months

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          Abstract

          Background

          Glucose is widely used as an osmotic agent in peritoneal dialysis (PD), but exerts untoward effects on the peritoneum. The potential protective effect of a reduced exposure to hypertonic glucose has never been investigated.

          Methods

          The cohort of PD patients attending our center which tackled the challenge of a restricted use of hypertonic glucose solutions has been prospectively followed since 1992. Small-solute transport was assessed using an equivalent of the glucose peritoneal equilibration test after 6 months, and then every year. Study was stopped on July 1st, 2008, before use of biocompatible solutions. Repeated measures in patients treated with PD for 54 months were analyzed by using (1) the slopes of the linear regression for D 4/D 0 ratios over time computed for each individual, and (2) a linear mixed model.

          Results

          In the study period, 44 patients were treated for a total of 2376 months, 2058 without hypertonic glucose. There was one episode of peritoneal infection every 18 patient-months. The mean of slopes of the linear regression for D 4/D 0 ratios was found to be significantly positive (Student’s test, p < .001) and the results of the mixed model reflected a similar significant increase for D 4/D 0 ratios over time. These results reflected a significant decrease of small-solute transport.

          Conclusion

          In this large series, minimizing the use of hypertonic glucose solutions was associated in patients on long term PD with an overall decrease of small-solute transport within 54 months, despite a high rate of peritoneal infection.

          Electronic supplementary material

          The online version of this article (10.1186/s12882-017-0690-7) contains supplementary material, which is available to authorized users.

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          Most cited references21

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          Peritoneal glucose exposure and changes in membrane solute transport with time on peritoneal dialysis.

          M. Davies, David Russell, Andrew Phillips … (2001)
          Peritoneal solute transport increases with time on treatment in a proportion of peritoneal dialysis (PD) patients, contributing to ultrafiltration failure. Continuous exposure of the peritoneum to hypertonic glucose solutions results in morphologic damage that may have a causative role in changes in peritoneal function. The purpose of this analysis was to establish whether increased exposure to glucose preceded changes in solute transport in a selected group of long-term PD patients. Peritoneal solute transport, residual renal function, peritonitis rate, and peritoneal exposure to glucose were recorded prospectively in a cohort of 303 patients at a single dialysis center. A subgroup of individuals, treated continuously for 5 yr, were identified and defined retrospectively as having either stable or increasing transport status. Of the 22 patients who were treated continuously for 5 yr, 13 had stable solute transport (solute transport at start, 0.67 [+/-0.1]; at 5 yr, 0.67 [+/-0.1]), whereas 9 had a sustained increase (solute transport at start, 0.56 [+/-0.08]; at 5 yr, 0.77 [+/-0.09]). Compared with the stable patients, those with increasing transport had earlier loss in residual renal function and were exposed to significantly more hypertonic glucose during the first 2 yr of treatment that preceded the increase in solute transport. This was associated with greater achieved ultrafiltration compensating for the reduced urinary volumes in these patients. Further increases in glucose exposure were observed as solute transport continued to rise. Peritonitis, including severity of infection and causative organism, was similar in both groups. In this selected group of long-term survivors on PD, an increase in solute transport with time was preceded by increased peritoneal exposure to hypertonic glucose. This is supportive evidence that hypertonic glucose may play a causative role in alterations in peritoneal membrane function.
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            What really happens to people on long-term peritoneal dialysis?

            Andrew Phillips, P L Naish, Melanie Davies … (1998)
            Several risk factors for patients treated with peritoneal dialysis (PD) have now been identified. These include age, comorbid disease, nutritional status, loss of residual renal function (RRF) and high peritoneal solute transport. This is not the same, however, as knowing what actually happens to these patients, particularly in the long-term. The purpose of this review was to give as complete a description as is currently possible of the long-term PD patient. The literature was surveyed for publications that provide longitudinal cohort data of either selected or unselected patient groups. Detailed data from the Stoke PD Study is presented in the context of these studies. Three principle aspects of what really happens to patients were considered: (1) death, both cause and mode of death; (2) technique failure, with reference to peritoneal function and how the cause of technique failure related to patient survival; and (3) evolution of clinically relevant parameters of patients on PD, such as nutrition and peritoneal function. Sudden death and debilitation were the predominant modes of death, with sepsis playing a contributory role. Debilitation was important regardless of co-existent comorbid disease, and time to death was not influenced by the mode of death. Predominant causes for technique failure remain peritonitis and ultrafiltration, the latter becoming more important with time on treatment. Technical failure is associated with poorer survival, particularly when due to multiple peritonitis or failure to cope with treatment. Cox regression demonstrated that whereas low albumin, loss of RRF and high solute transport predicted patient death, only high solute transport predicted technique failure. Longitudinal changes over the first five years of treatment included loss of RRF, increasing solute transport and following an initial improvement in nutritional state, a decline after two years. Patients surviving long-term PD (at least five years, N = 25) were characterized by prolonged RRF, maintained nutrition and lower solute transport in the medium term. Several studies of long-term PD in the literature now complement each other in providing a picture of what really happens to PD patients. The links between loss of solute clearance and poor peritoneal ultrafiltration combining to exacerbate sudden or debilitated death and technique failure are emerging. For PD to be successful as a long-term therapy, strategies that maintain nutrition and preserve peritoneal membrane function must be developed.
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              The Euro-Balance Trial: the effect of a new biocompatible peritoneal dialysis fluid (balance) on the peritoneal membrane.

              John Williams, Nicholas Topley, Kathrine Craig … (2004)
              Although peritoneal dialysis (PD) is a widely accepted form of renal replacement therapy (RRT), concerns remain regarding the bioincompatible nature of standard PD fluid. In order to evaluate whether a newly formulated fluid of neutral pH, and containing low levels of glucose degradation products (GDP), resulted in improved in vivo biocompatibility, it was compared in a clinical study to a standard PD fluid. In a multicenter, open, randomized, prospective study with a crossover design and parallel arms, a conventional, acidic, lactate-buffered fluid (SPDF) was compared with a pH neutral, lactate-buffered, low GDP fluid (balance). Overnight effluent was collected and assayed for cancer antigen 125 (CA125), hyaluronic acid (HA), procollagen peptide (PICP), vascular endothelial growth factor (VEGF), and tumor necrosis factor alpha (TNFalpha). Serum samples were assayed for circulating advanced glycosylation end products (AGE), N(epsilon)-(carboxymethyl)lysine (CML), and imidazolone. Clinical end points were residual renal function (RRF), adequacy of dialysis, ultrafiltration, and peritoneal membrane function. Eighty-six patients were randomized to either group I starting with SPDF for 12 weeks (Phase I), then switching to "balance" for 12 weeks (Phase II), or group II, which was treated vice versa. Seventy-one patients completed the study with data suitable for entry into the per protocol analysis. Effluent and serum samples, together with peritoneal function tests and adequacy measurements, were undertaken at study centers on three occasions during the study: after the four-week run-in period, after Phase I, and again after Phase II. In patients treated with balance there were significantly higher effluent levels of CA125 and PICP in both arms of the study. Conversely, levels of HA were lower in patients exposed to balance, while there was no change in the levels of either VEGF or TNFalpha. Serum CML and imidazolone levels fell significantly in balance-treated patients. Renal urea and creatinine clearances were higher in both treatment arms after patients were exposed to balance. Urine volume was higher in patients exposed to balance. In contrast, peritoneal ultrafiltration was higher in patients on SPDF. When anuric patients were analyzed as a subgroup, there was no significant difference in peritoneal transport characteristics or in ultrafiltration on either fluid. There were no changes in peritonitis incidence on either solution. This study indicates that the use of balance, a neutral pH, low GDP fluid, is accompanied by a significant improvement in effluent markers of peritoneal membrane integrity and significantly decreased circulating AGE levels. Clinical parameters suggest an improvement in residual renal function on balance, with an accompanying decrease in peritoneal ultrafiltration. It would appear that balance solution results in an improvement in local peritoneal homeostasis, as well as having a positive impact on systemic parameters, including circulating AGE and residual renal function.
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                Author and article information

                Contributors
                Dominique Pagniez: dpagniez@chru-lille.fr
                Alain Duhamel: alain.duhamel@univ-lille2.fr
                Eric Boulanger: dreboulanger@hotmail.com
                Celia Lessore de Sainte Foy: c.lessore@gmail.com
                Jean-Baptiste Beuscart:
                ORCID: http://orcid.org/0000-0002-0734-8371
                +33 3 2062 6969 , jean-baptiste.beuscart@univ-lille2.fr
                Journal
                Journal ID (nlm-ta): BMC Nephrol
                Journal ID (iso-abbrev): BMC Nephrol
                Title: BMC Nephrology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2369
                Publication date (Electronic): 31 August 2017
                Publication date PMC-release: 31 August 2017
                Publication date Collection: 2017
                Volume: 18
                Electronic Location Identifier: 278
                Affiliations
                [1 ]ISNI 0000 0004 0471 8845, GRID grid.410463.4, CHU Lille, Nephrology Department, ; F-59000 Lille, France
                [2 ]Univ. Lille, EA 2694 - Santé publique: épidémiologie et qualité des soins, F-59000 Lille, France
                [3 ]ISNI 0000 0004 0471 8845, GRID grid.410463.4, Univ. Lille, Inserm, CHU Lille, U995 - LIRIC - Lille Inflammation Research International Center, ; F-59000 Lille, France
                Author information
                http://orcid.org/0000-0002-0734-8371
                Article
                Publisher ID: 690
                DOI: 10.1186/s12882-017-0690-7
                PMC ID: 5580320
                PubMed ID: 28859606
                SO-VID: 8aea5e17-baff-4688-aac1-c96ee90f168d
                Copyright © © The Author(s). 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 9 March 2016
                Date accepted : 17 August 2017
                Funding
                Funded by: a Clinical Evidence Council (CEC) grant from Baxter Healthcare Corporation (Deerfield, IL)
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Nephrology
                Keywords: glucose exposure,glucose sparing,small-solute transport,peritoneal dialysis,peritoneal equilibration test
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: glucose exposure, glucose sparing, small-solute transport, peritoneal dialysis, peritoneal equilibration test

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