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• W1976159601 abstract "For patients on peritoneal dialysis (PD), the development of peritonitis, the decline of residual kidney function, and the loss of peritoneal membrane function are central events that affect both patient and technique survival. The use of glucose as the osmotic agent in conventional PD solutions may increase the susceptibility to each of these events. However, its use may also be associated with systemic metabolic perturbations and, in turn, an increase in cardiovascular morbidity. Both in vitro and in vivo evidence suggest that both the local peritoneal and systemic toxicity induced by the use of glucose may be in part mediated by the presence of glucose degradation products (GDPs) coupled with the hyperosmolarity, reduced pH, and use of lactate as the buffer in conventional PD solutions. Therefore, the use of neutral pH, low-GDP (NpHLGDP), bicarbonate-buffered PD solutions may represent a promising strategy to attenuate some of these adverse effects. However, the impact of these novel solutions on clinical outcomes remains largely unknown. In this review, we will highlight evidence regarding the biocompatibility of NpHLGDP PD solutions, review the utility of current biomarkers in the evaluation of biocompatibility, and discuss the clinical outcome data with these solutions. For patients on peritoneal dialysis (PD), the development of peritonitis, the decline of residual kidney function, and the loss of peritoneal membrane function are central events that affect both patient and technique survival. The use of glucose as the osmotic agent in conventional PD solutions may increase the susceptibility to each of these events. However, its use may also be associated with systemic metabolic perturbations and, in turn, an increase in cardiovascular morbidity. Both in vitro and in vivo evidence suggest that both the local peritoneal and systemic toxicity induced by the use of glucose may be in part mediated by the presence of glucose degradation products (GDPs) coupled with the hyperosmolarity, reduced pH, and use of lactate as the buffer in conventional PD solutions. Therefore, the use of neutral pH, low-GDP (NpHLGDP), bicarbonate-buffered PD solutions may represent a promising strategy to attenuate some of these adverse effects. However, the impact of these novel solutions on clinical outcomes remains largely unknown. In this review, we will highlight evidence regarding the biocompatibility of NpHLGDP PD solutions, review the utility of current biomarkers in the evaluation of biocompatibility, and discuss the clinical outcome data with these solutions. Central to the success of peritoneal dialysis (PD) is the long-term preservation of the peritoneal membrane. In contrast to hemodialysis (HD) in which the specifications of the dialyzer are known and can be altered, the peritoneal membrane is a biological membrane and susceptible to injury. Peritoneal membrane changes seen with increasing duration on PD include fibrosis, and both quantitative and qualitative changes within the peritoneal microcirculation.1.Williams J.D. Craig K.J. Topley N. et al.Morphologic changes in the peritoneal membrane of patients with renal disease.J Am Soc Nephrol. 2002; 13: 470-479PubMed Google Scholar These changes correlate with increasing small-solute permeability and a reduction in peritoneal ultrafiltration (UF) capacity,2.Plum J. Hermann S. Fussholler A. et al.Peritoneal sclerosis in peritoneal dialysis patients related to dialysis settings and peritoneal transport properties.Kidney Int Suppl. 2001; 78: S42-S47Crossref PubMed Google Scholar, 3.Numata M. Nakayama M. Nimura S. et al.Association between an increased surface area of peritoneal microvessels and a high peritoneal solute transport rate.Perit Dial Int. 2003; 23: 116-122PubMed and may be partially responsible for the shortened technique survival of PD relative to HD.4.Serkes K.D. Blagg C.R. Nolph K.D. et al.Comparison of patient and technique survival in continuous ambulatory peritoneal dialysis (CAPD) and hemodialysis: a multicenter study.Perit Dial Int. 1990; 10: 15-19PubMed Google Scholar, 5.Maiorca R. Vonesh E. Cancarini G.C. et al.A six-year comparison of patient and technique survivals in CAPD and HD.Kidney Int. 1988; 34: 518-524Abstract Full Text PDF PubMed Scopus (109) Google Scholar The observation that these deleterious changes occurred under conditions of chronic exposure to conventional hyperosmolar glucose-containing, lactate-buffered, low-pH PD solutions has led to the conclusion that the composition of conventional PD solutions is responsible. If dialysate incompatibility contributes to technique failure, then manipulation of conventional PD solution composition represents a therapeutic target to improve patient outcomes on PD. Possible strategies include the use of non-glucose-based PD solutions, or, alternatively, modification of other dialysate components to minimize the local peritoneal and systemic toxicity imposed by glucose. The latter strategy involves the use of glucose-based, neutral pH, low glucose degradation product (NpHLGDP) PD solutions to minimize the toxicity mediated by GDPs and low pH. Both ex vivo and animal data provide convincing evidence that peritoneal and systemic exposure to GDP and low pH have been linked to peritoneal membrane injury, impairment of local peritoneal host defenses, renal injury, and systemic inflammation. We will summarize the current knowledge regarding the bioincompatibility of conventional PD solutions, while highlighting the variability in the composition of commercially available, NpHLGDP PD solutions. The impact of these solutions on clinical outcomes, including peritoneal membrane function, preservation of residual kidney function (RKF), PD-related infectious complications, as well as patient and technique survival will be presented. Heat (autoclave) sterilization of conventional glucose-based PD solutions has given rise to elevated levels of dialysate GDPs that are produced during both manufacturing and storage.6.Martis L. Henderson L.W. Impact of terminal heat sterilization on the quality of peritoneal dialysis solutions.Blood Purif. 1997; 15: 54-60Crossref PubMed Scopus (13) Google Scholar, 7.Nilsson-Thorell C.B. Muscalu N. Andren A.H. et al.Heat sterilization of fluids for peritoneal dialysis gives rise to aldehydes.Perit Dial Int. 1993; 13: 208-213PubMed Google Scholar To reduce this caramelization of glucose, it is buffered with lactate and the solution is maintained at a low pH (5.0–6.0).6.Martis L. Henderson L.W. Impact of terminal heat sterilization on the quality of peritoneal dialysis solutions.Blood Purif. 1997; 15: 54-60Crossref PubMed Scopus (13) Google Scholar In contrast, NpHLGDP PD solutions have a final pH of approximately 6.2–7.4. The use of a multi-bag system allows for separation into two compartments: a low-pH glucose compartment, which minimizes the production of GDPs during heat sterilization and storage,8.Cooker L.A. Luneburg P. Faict D. et al.Reduced glucose degradation products in bicarbonate/lactate-buffered peritoneal dialysis solutions produced in two-chambered bags.Perit Dial Int. 1997; 17: 373-378PubMed Google Scholar, 9.Kjellstrand P. Martinson E. Wieslander A. et al.Degradation in peritoneal dialysis fluids may be avoided by using low pH and high glucose concentration.Perit Dial Int. 2001; 21: 338-344PubMed Google Scholar and a buffer compartment, which can be lactate, a bicarbonate/lactate mixture, or bicarbonate alone (Table 1). This also separates calcium from bicarbonate, avoiding precipitation of the two until both compartments are mixed immediately before instillation. The final GDP content and type varies by solution and manufacturer10.Erixon M. Wieslander A. Linden T. et al.How to avoid glucose degradation products in peritoneal dialysis fluids.Perit Dial Int. 2006; 26: 490-497PubMed Google Scholar (Figure 1).Table 1Commercially available, neutral pH, low-GDP peritoneal dialysis solutions and conventional peritoneal dialysis solutionBuffer (mmol/l)ChambersLactateBicarbonateFinal pHBalance235—6.8Bicavera2—34/397.1Gambrosol Trio3aChambers to allow for final glucose concentration of three different concentrations.39–41—6.5Physioneal210/15257.3Conventional135/40—5.0–5.4Abbreviation: GDP, glucose degradation product.a Chambers to allow for final glucose concentration of three different concentrations. Open table in a new tab Abbreviation: GDP, glucose degradation product. Uremia initiates structural peritoneal membrane changes that are exacerbated with increasing duration on PD.1.Williams J.D. Craig K.J. Topley N. et al.Morphologic changes in the peritoneal membrane of patients with renal disease.J Am Soc Nephrol. 2002; 13: 470-479PubMed Google Scholar Peritoneal biopsy registry data suggest that these changes are seen across all resident cells of the peritoneum.1.Williams J.D. Craig K.J. Topley N. et al.Morphologic changes in the peritoneal membrane of patients with renal disease.J Am Soc Nephrol. 2002; 13: 470-479PubMed Google Scholar These changes include the loss of the mesothelial monolayer, thickening of the submesothelial compact collagenous zone, neovascularization, and additional vascular changes including subendothelial hyalinization of post-capillary venules, with accompanying obliteration or narrowing of the vascular lumen.1.Williams J.D. Craig K.J. Topley N. et al.Morphologic changes in the peritoneal membrane of patients with renal disease.J Am Soc Nephrol. 2002; 13: 470-479PubMed Google Scholar Ultrastructurally, ‘diabetiform’ vascular changes are observed, including lamellation of the capillary and mesothelial basement membrane.11.Gotloib L. Bar-Sella P. Shostak A. Reduplicated basal lamina of small venules and mesothelium of human parietal peritoneum: ultrastructural changes of reduplicated peritoneal basement membrane.Perit Dial Int. 1985; 5: 212-214Google Scholar, 12.Dobbie J.W. Anderson J.D. Hind C. Long-term effects of peritoneal dialysis on peritoneal morphology.Perit Dial Int. 1994; 14: S16-S20PubMed Google Scholar, 13.Di Paolo N. Sacchi G. Peritoneal vascular changes in continuous ambulatory peritoneal dialysis (CAPD): an in vivo model for the study of diabetic microangiopathy.Perit Dial Int. 1989; 9: 41-45PubMed Google Scholar, 14.Mateijsen M.A. van der Wal A.C. Hendriks P.M. et al.Vascular and interstitial changes in the peritoneum of CAPD patients with peritoneal sclerosis.Perit Dial Int. 1999; 19: 517-525PubMed Google Scholar These changes raise the possibility that the presence of glucose in conventional PD solutions may be mediating these deleterious effects. Similar changes have been reproduced in animal models exposed to hypertonic, glucose-based dialysate.15.Duman S. Gunal A.I. Sen S. et al.Does enalapril prevent peritoneal fibrosis induced by hypertonic (3.86%) peritoneal dialysis solution?.Perit Dial Int. 2001; 21: 219-224PubMed Google Scholar Moreover, glucose also has a dose-dependent inhibitory effect on mesothelial cell proliferation in human and animal models.16.Shao J.C. Yorioka N. Nishida Y. et al.Effect of pH and glucose on cultured human peritoneal mesothelial cells.Scand J Urol Nephrol. 1999; 33: 248-256Crossref PubMed Scopus (19) Google Scholar, 17.Boulanger E. Wautier M.P. Gane P. et al.The triggering of human peritoneal mesothelial cell apoptosis and oncosis by glucose and glycoxydation products.Nephrol Dial Transplant. 2004; 19: 2208-2216Crossref PubMed Scopus (70) Google Scholar, 18.Ciszewicz M. Wu G. Tam P. et al.Changes in peritoneal mesothelial cells phenotype after chronic exposure to glucose or N-acetylglucosamine.Transl Res. 2007; 150: 337-342Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar, 19.Di Paolo N. Garosi G. Petrini G. et al.Morphological and morphometric changes in mesothelial cells during peritoneal dialysis in the rabbit.Nephron. 1996; 74: 594-599Crossref PubMed Scopus (26) Google Scholar This toxicity may be mediated by oxidative stress.18.Ciszewicz M. Wu G. Tam P. et al.Changes in peritoneal mesothelial cells phenotype after chronic exposure to glucose or N-acetylglucosamine.Transl Res. 2007; 150: 337-342Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar Mitochondrial DNA damage has been demonstrated on exposure of human peritoneal mesothelial cells (HPMCs) to glucose.20.Ishibashi Y. Sugimoto T. Ichikawa Y. et al.Glucose dialysate induces mitochondrial DNA damage in peritoneal mesothelial cells.Perit Dial Int. 2002; 22: 11-21PubMed Google Scholar Compared with other hyperosmolar solutes such as mannitol and glycerol, the inhibitory effects of glucose on mesothelial cells seems to be greater, implying both an effect of hyperosmolality and an intrinsic toxic effect of glucose on mesothelial cell proliferation.21.Breborowicz A. Rodela H. Oreopoulos D.G. Toxicity of osmotic solutes on human mesothelial cells in vitro.Kidney Int. 1992; 41: 1280-1285Abstract Full Text PDF PubMed Scopus (124) Google Scholar Evidence that these glucose-induced structural changes translate into adverse effects on membrane function stems from a single-center observational cohort study by Davies et al.22.Davies S.J. Phillips L. Naish P.F. et al.Peritoneal glucose exposure and changes in membrane solute transport with time on peritoneal dialysis.J Am Soc Nephrol. 2001; 12: 1046-1051PubMed Google Scholar In this study, patients with greater early and cumulative exposure to higher glucose concentrations experienced more rapid increases in small-solute permeability and faster deterioration of membrane function. However, the possibility that the need for higher dialysate glucose exposure may have been in response to declining RKF or to inadequate peritoneal UF, in the face of worsening peritoneal membrane function, cannot be excluded. In 1986, the observation by Henderson et al.23.Henderson I.S. Couper L.A. Lumsden A. The effect of shelf-life of peritoneal dialysis fluid on ultrafiltration in CAPD.in: La Greca G. Chiaramonte S. Fabris A. Feriani M. Ronco C. Proceedings of the Second International Course on Peritoneal Dialysis. Wichtig Editore, Milan1986: 85-86Google Scholar that PD infusion pain correlated with the shelf life of the PD solution being infused ultimately gave rise to the discovery of GDPs in conventional PD solutions. The shelf life of the conventional dialysis solutions was found to correlate with increasing GDP content, as detected by photospectrometric analysis.23.Henderson I.S. Couper L.A. Lumsden A. The effect of shelf-life of peritoneal dialysis fluid on ultrafiltration in CAPD.in: La Greca G. Chiaramonte S. Fabris A. Feriani M. Ronco C. Proceedings of the Second International Course on Peritoneal Dialysis. Wichtig Editore, Milan1986: 85-86Google Scholar Since that time, increasing evidence from in vitro and animal studies suggests that the local toxicity of glucose may be, in part, related to the presence of GDPs in conventional PD solutions. To date, the majority of evidence surrounding the peritoneal toxicity of GDPs has focused on the effects of GDPs on mesothelial cell injury.24.Witowski J. Wisniewska J. Korybalska K. et al.Prolonged exposure to glucose degradation products impairs viability and function of human peritoneal mesothelial cells.J Am Soc Nephrol. 2001; 12: 2434-2441PubMed Google Scholar Only a few of these low-molecular-weight aldehydes have been identified, with several more GDPs visible by high-performance liquid chromatography.7.Nilsson-Thorell C.B. Muscalu N. Andren A.H. et al.Heat sterilization of fluids for peritoneal dialysis gives rise to aldehydes.Perit Dial Int. 1993; 13: 208-213PubMed Google Scholar Initial reports suggested that the acute cellular toxicity due to GDPs was only achievable at high concentrations, exceeding those found in PD fluids.25.Witowski J. Korybalska K. Wisniewska J. et al.Effect of glucose degradation products on human peritoneal mesothelial cell function.J Am Soc Nephrol. 2000; 11: 729-739PubMed Google Scholar, 26.Witowski J. Jorres A. Glucose degradation products: relationship with cell damage.Perit Dial Int. 2000; 20: S31-S36PubMed Google Scholar, 27.Wieslander A.P. Andren A.H. Nilsson-Thorell C. et al.Are aldehydes in heat-sterilized peritoneal dialysis fluids toxic in vitro?.Perit Dial Int. 1995; 15: 348-352PubMed Google Scholar However, the discovery of the GDP, 3,4-dideoxyglucosone-3-ene (3,4-DGE), confirmed that concentrations of 3,4-DGE found in conventional PD fluid could induce acute cellular toxicity using an in vitro fibroblast culture model.28.Linden T. Cohen A. Deppisch R. et al.3,4-Dideoxyglucosone-3-ene (3,4-DGE): a cytotoxic glucose degradation product in fluids for peritoneal dialysis.Kidney Int. 2002; 62: 697-703Abstract Full Text Full Text PDF PubMed Scopus (119) Google Scholar Given the nature of the cell lines used and the short duration of incubation in previous studies (<72 h), specific conclusions regarding in vivo long-term peritoneal effects remained limited. Using a culture of omental-derived HPMCs, Witowski et al.24.Witowski J. Wisniewska J. Korybalska K. et al.Prolonged exposure to glucose degradation products impairs viability and function of human peritoneal mesothelial cells.J Am Soc Nephrol. 2001; 12: 2434-2441PubMed Google Scholar demonstrated that exposure to six GDPs in concentrations typically found in conventional PD solution was not associated with short-term toxicity. However, after 6 weeks of exposure, the viability and function of the HPMCs was severely comprised. It would appear that not all GDPs have an equivalent capability for mesothelial cell toxicity.29.Lee D.H. Choi S.Y. Ryu H.M. et al.3,4-Dideoxyglucosone-3-ene induces apoptosis in human peritoneal mesothelial cells.Perit Dial Int. 2009; 29: 44-51PubMed Google Scholar 3,4-DGE has been shown to be among the most inhibitory for mesothelial cell proliferation, and is also the only GDP that has been demonstrated to enhance apoptosis of both peripheral leukocytes as well as renal tubular epithelial cells.29.Lee D.H. Choi S.Y. Ryu H.M. et al.3,4-Dideoxyglucosone-3-ene induces apoptosis in human peritoneal mesothelial cells.Perit Dial Int. 2009; 29: 44-51PubMed Google Scholar, 30.Justo P. Sanz A.B. Egido J. et al.3,4-Dideoxyglucosone-3-ene induces apoptosis in renal tubular epithelial cells.Diabetes. 2005; 54: 2424-2429Crossref PubMed Scopus (82) Google Scholar, 31.Catalan M.P. Santamaria B. Reyero A. et al.3,4-Di-deoxyglucosone-3-ene promotes leukocyte apoptosis.Kidney Int. 2005; 68: 1303-1311Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar In addition, 3,4-DGE and formaldehyde are among the most potent GDPs responsible for impairment in mesothelial cell repair in response to injury.32.Morgan L.W. Wieslander A. Davies M. et al.Glucose degradation products (GDP) retard remesothelialization independently of D-glucose concentration.Kidney Int. 2003; 64: 1854-1866Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar GDP-induced mesothelial cell injury and apoptosis also lead to intracellular hydrogen peroxide production and free radical formation, which may be important inciting events for peritoneal membrane inflammation and injury.33.Shostak A. Pivnik E. Gotloib L. Cultured rat mesothelial cells generate hydrogen peroxide: a new player in peritoneal defense?.J Am Soc Nephrol. 1996; 7: 2371-2378PubMed Google Scholar, 34.Noh H. Kim J.S. Han K.H. et al.Oxidative stress during peritoneal dialysis: implications in functional and structural changes in the membrane.Kidney Int. 2006; 69: 2022-2028Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar Moreover, GDPs have been shown to directly induce production of the profibrotic cytokine transforming growth factor-β and to stimulate vascular endothelial growth factor (VEGF) synthesis in HPMCs.35.Kang D.H. Hong Y.S. Lim H.J. et al.High glucose solution and spent dialysate stimulate the synthesis of transforming growth factor-beta1 of human peritoneal mesothelial cells: effect of cytokine costimulation.Perit Dial Int. 1999; 19: 221-230PubMed Google Scholar, 36.Ha H. Yu M.R. Lee H.B. High glucose-induced PKC activation mediates TGF-beta 1 and fibronectin synthesis by peritoneal mesothelial cells.Kidney Int. 2001; 59: 463-470Abstract Full Text Full Text PDF PubMed Scopus (143) Google Scholar, 37.Inagi R. Miyata T. Yamamoto T. et al.Glucose degradation product methylglyoxal enhances the production of vascular endothelial growth factor in peritoneal cells: role in the functional and morphological alterations of peritoneal membranes in peritoneal dialysis.FEBS Lett. 1999; 463: 260-264Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar, 38.Leung J.C. Chan L.Y. Li F.F. et al.Glucose degradation products downregulate ZO-1 expression in human peritoneal mesothelial cells: the role of VEGF.Nephrol Dial Transplant. 2005; 20: 1336-1349Crossref PubMed Scopus (47) Google Scholar, 39.Seo M.J. Oh S.J. Kim S.I. et al.High glucose dialysis solutions increase synthesis of vascular endothelial growth factors by peritoneal vascular endothelial cells.Perit Dial Int. 2001; 21: S35-S40PubMed Google Scholar These two signaling molecules are thought to have key roles in the progressive peritoneal membrane fibrosis and vascular proliferation seen in long-term PD patients.40.De Vriese A.S. Tilton R.G. Stephan C.C. et al.Vascular endothelial growth factor is essential for hyperglycemia-induced structural and functional alterations of the peritoneal membrane.J Am Soc Nephrol. 2001; 12: 1734-1741PubMed Google Scholar In a rat model, exposure to GDPs has also been shown to stimulate excessive proliferation of mesenchymal-like cells.41.Hirahara I. Ishibashi Y. Kaname S. et al.Methylglyoxal induces peritoneal thickening by mesenchymal-like mesothelial cells in rats.Nephrol Dial Transplant. 2009; 24: 437-447Crossref PubMed Scopus (47) Google Scholar These cells may be derived through epithelial–mesenchymal transition (EMT), whereby peritoneal mesothelial cells undergo transition to a fibroblast-like phenotype and is thought to be a key mediator of peritoneal fibrosis.42.Yanez-Mo M. Lara-Pezzi E. Selgas R. et al.Peritoneal dialysis and epithelial-to-mesenchymal transition of mesothelial cells.N Engl J Med. 2003; 348: 403-413Crossref PubMed Scopus (577) Google Scholar Whether or not proliferation of mesenchymal cells is directly stimulated by exposure to GDPs or indirectly by GDP-induced upregulation of transforming growth factor-β (a known stimulus for EMT) is unclear.42.Yanez-Mo M. Lara-Pezzi E. Selgas R. et al.Peritoneal dialysis and epithelial-to-mesenchymal transition of mesothelial cells.N Engl J Med. 2003; 348: 403-413Crossref PubMed Scopus (577) Google Scholar Dialysate effluent obtained from patients at 12 months after the initiation of PD using low-GDP solutions contained fewer fibroblast-dominant cells compared with the effluent obtained from patients using conventional PD solutions, suggesting GDP-induced EMT in vivo.43.Do J.Y. Kim Y.L. Park J.W. et al.The effect of low glucose degradation product dialysis solution on epithelial-to-mesenchymal transition in continuous ambulatory peritoneal dialysis patients.Perit Dial Int. 2005; 25: S22-S25PubMed Google Scholar Taken together, in vitro and animal data suggest that peritoneal mesothelial cell integrity may be adversely affected by the presence of GDPs in conventional PD solution. The alterations in mesothelial cell viability may initiate a cascade of events, leading to progressive peritoneal membrane injury. Under conditions of elevated glucose, advanced glycosylation end products (AGE) are formed from the non-enzymatic glycosylation of proteins.44.Brownlee M. Cerami A. Vlassara H. Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications.N Engl J Med. 1988; 318: 1315-1321Crossref PubMed Scopus (2271) Google Scholar AGEs have the potential to increase vascular permeability by disruption of the vascular basement membrane due to protein cross-linking to basement membrane components45.Charonis A.S. Reger L.A. Dege J.E. et al.Laminin alterations after in vitro nonenzymatic glycosylation.Diabetes. 1990; 39: 807-814Crossref PubMed Google Scholar or by the activation of the receptor for AGEs (RAGE) on endothelial cells.46.Esposito C. Gerlach H. Brett J. et al.Endothelial receptor-mediated binding of glucose-modified albumin is associated with increased monolayer permeability and modulation of cell surface coagulant properties.J Exp Med. 1989; 170: 1387-1407Crossref PubMed Scopus (335) Google Scholar In vitro kinetic studies suggest that the formation of AGEs on exposure to conventional PD solutions appears to be largely mediated by the presence of GDPs.47.Lamb E.J. Cattell W.R. Dawnay A.B. In vitro formation of advanced glycation end products in peritoneal dialysis fluid.Kidney Int. 1995; 47: 1768-1774Abstract Full Text PDF PubMed Scopus (90) Google Scholar GDPs appear to have greater reactivity than glucose in the formation of AGEs and incubation with NpHLGDP PD solutions results in lower systemic AGE levels compared with conventional PD solutions incubated at similar concentrations of glucose.48.Zeier M. Schwenger V. Deppisch R. et al.Glucose degradation products in PD fluids: do they disappear from the peritoneal cavity and enter the systemic circulation?.Kidney Int. 2003; 63: 298-305Abstract Full Text Full Text PDF PubMed Scopus (147) Google Scholar, 49.Schmitt C.P. von Heyl D. Rieger S. et al.Reduced systemic advanced glycation end products in children receiving peritoneal dialysis with low glucose degradation product content.Nephrol Dial Transplant. 2007; 22: 2038-2044Crossref PubMed Scopus (45) Google Scholar Moreover, in peritoneal effluent, AGEs have been detected at levels greater than plasma, and appreciable staining for AGEs has been demonstrated in the peritoneal membrane as early as within the first 3 months of PD therapy.50.Friedlander M.A. Wu Y.C. Elgawish A. et al.Early and advanced glycosylation end products. Kinetics of formation and clearance in peritoneal dialysis.J Clin Invest. 1996; 97: 728-735Crossref PubMed Scopus (106) Google Scholar, 51.Yamada K. Miyahara Y. Hamaguchi K. et al.Immunohistochemical study of human advanced glycosylation end-products (AGE) in chronic renal failure.Clin Nephrol. 1994; 42: 354-361PubMed Rat models suggest that accelerated AGE formation may have a causative role in PD solution-induced peritoneal membrane injury.52.Mortier S. Faict D. Schalkwijk C.G. et al.Long-term exposure to new peritoneal dialysis solutions: effects on the peritoneal membrane.Kidney Int. 2004; 66: 1257-1265Abstract Full Text Full Text PDF PubMed Scopus (154) Google Scholar In these models, increased peritoneal deposition of GDPs and AGEs and upregulation of the RAGE are seen with exposure to conventional PD solutions compared with NpHLGDP solutions.52.Mortier S. Faict D. Schalkwijk C.G. et al.Long-term exposure to new peritoneal dialysis solutions: effects on the peritoneal membrane.Kidney Int. 2004; 66: 1257-1265Abstract Full Text Full Text PDF PubMed Scopus (154) Google Scholar Structurally, these changes are accompanied by increases in submesothelial fibrosis, VEGF production, and microvascular proliferation, while functional changes include lower peritoneal UF.52.Mortier S. Faict D. Schalkwijk C.G. et al.Long-term exposure to new peritoneal dialysis solutions: effects on the peritoneal membrane.Kidney Int. 2004; 66: 1257-1265Abstract Full Text Full Text PDF PubMed Scopus (154) Google Scholar RAGE has also been detected on the surface of HPMCs.53.Lai K.N. Leung J.C. Chan L.Y. et al.Differential expression of receptors for advanced glycation end-products in peritoneal mesothelial cells exposed to glucose degradation products.Clin Exp Immunol. 2004; 138: 466-475Crossref PubMed Scopus (38) Google Scholar Stimulation of RAGE by AGEs results in VEGF release by HPMCs, which leads to capillary tube formation of human umbilical vein endothelial cells in a co-culture model.54.Boulanger E. Grossin N. Wautier M.P. et al.Mesothelial RAGE activation by AGEs enhances VEGF release and potentiates capillary tube formation.Kidney Int. 2007; 71: 126-133Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar This may be an important mechanism underlying the angiogenesis of the peritoneal capillary network seen in long-term PD.54.Boulanger E. Grossin N. Wautier M.P. et al.Mesothelial RAGE activation by AGEs enhances VEGF release and potentiates capillary tube formation.Kidney Int. 2007; 71: 126-133Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Moreover, AGEs binding to RAGE on HPMCs also stimulate activation and upregulation of vascular cell adhesion molecule-1 on the mesothelial cell surface.55.Boulanger E. Wautier M.P. Wautier J.L. et al.AGEs bind to mesothelial cells via RAGE and stimulate VCAM-1 expression.Kidney Int. 2002; 61: 148-156Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholar Vascular cell adhesion molecule-1 has an integral role in facilitating leukocyte adhesion, which may activate an inflammatory pathway and lead to peritoneal injury.56.Carlos T.M. Harlan J.M. Leukocyte-endothelial adhesion molecules.Blood. 1994; 84: 2068-2101Crossref PubMed Google Scholar Human peritoneal biopsies suggest that AGE accumulation in the peritoneal membrane occurs predominantly in the vessel wall. AGE deposition correlates with increased time on therapy and increased peritoneal permeability.57.Nakayama M. Kawaguchi Y. Yamada K. et al.Immunohistochemical detection of advanced glycosylation end-products in the peritoneum and its possible pathophysiological role in CAPD.Kidney Int. 1997; 51: 182-186Abstract Full Text PDF PubMed Scopus (276) Google Scholar, 58.Honda K. Nitta K. Horita S. et al.Accumulation of advanced glycation end products in the peritone" @default.
• W1976159601 created "2016-06-24" @default.
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• W1976159601 date "2011-04-01" @default.
• W1976159601 modified "2023-10-12" @default.
• W1976159601 title "The biocompatibility of neutral pH, low-GDP peritoneal dialysis solutions: benefit at bench, bedside, or both?" @default.
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