Continuous Flow Peritoneal Dialysis: Solution Formulation and Biocompatibility

Passlick–Deetjen, Jutta; Lage, Cristina; Jörres, Achim

doi:10.1046/j.1525-139x.2001.00100.x

Cited by 12 publications

(5 citation statements)

References 40 publications

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“…Advanced glycation end-products (AGEs), which are believed to promote atherosclerosis through interaction with endothelial receptors [36], are commonly accumulated in CKD patients due to decreased renal clearance, could be overproduced in PD patients due to the high exposure to glucose and glucose degradation products (GDP). Bioincompatibility of conventional glucose-based peritoneal dialysis fluids (PDF) has been partially attributed to the presence of GDP generated during heat sterilization of PDF [37], [38], which are thought to contribute to cellular dysfunction and membrane damage during peritoneal dialysis [39], [35], [40]. In accordance with these previous results, our present study shows that the glucose load and the presence of GDP could play a role in the development of endothelial damage among these patients.…”

Section: Discussionsupporting

confidence: 85%

NFκB in the Development of Endothelial Activation and Damage in Uremia: An In Vitro Approach

et al. 2012

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Impaired hemostasis coexists with accelerated atherosclerosis in patients with chronic kidney disease (CKD). The elevated frequency of atherothrombotic events has been associated with endothelial dysfunction. The relative contribution of the uremic state and the impact of the renal replacement therapies have been often disregarded. Plasma markers of endothelial activation and damage were evaluated in three groups of patients with CKD: under conservative treatment (predialysis), on hemodialysis, and on peritoneal dialysis. Activation of p38 MAPK and the transcription factor NFκB was assessed in endothelial cell (EC) cultures exposed to pooled sera from each group of patients. Most of the markers evaluated (VCAM-1, ICAM-1, VWF, circulating endothelial cells) were significantly higher in CDK patients than in controls, being significantly more increased in the group of peritoneal dialysis patients. These results correlated with the activation of both p38 MAPK and NFκB in EC cells exposed to the same sera samples, and also to the peritoneal dialysis fluids. Hemodialysis did not further contribute to the endothelial damage induced by the uremic state observed in predialysis patients, probably due to the improved biocompatibility of the hemodialysis technique in recent years, resulting in lower cellular activation. However, peritoneal dialysis seemed to exert a significant proinflammatory effect on the endothelium that could be related to the high glucose concentrations and glucose degradation products present in the dialysis fluid. Although peritoneal dialysis has been traditionally considered a more physiological technique, our results raise some doubts with respect to inflammation and EC damage.

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Section: Discussionsupporting

confidence: 85%

NFκB in the Development of Endothelial Activation and Damage in Uremia: An In Vitro Approach

et al. 2012

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“…168 PD, an important alternative to HD, also reduces AGEs formation. 169,170 Advantageously, serum concentrations of AGEs, such as pentosidine, are lower in patients on PD than in patients on HD. 171 However, despite higher levels of AGE excretion in patients on PD, free AGE levels in the PD effluent were elevated because of increased synthesis of free AGEs.…”

Section: Inhibition Of Gastrointestinal Absorptionmentioning

confidence: 99%

Uremic Toxicity of Advanced Glycation End Products in CKD

Stinghen

Massy

Vlassara

et al. 2016

Journal of the American Society of Nephrology

195

175

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Advanced glycation end products (AGEs), a heterogeneous group of compounds formed by nonenzymatic glycation reactions between reducing sugars and amino acids, lipids, or DNA, are formed not only in the presence of hyperglycemia, but also in diseases associated with high levels of oxidative stress, such as CKD. In chronic renal failure, higher circulating AGE levels result from increased formation and decreased renal clearance. Interactions between AGEs and their receptors, including advanced glycation end product-specific receptor (RAGE), trigger various intracellular events, such as oxidative stress and inflammation, leading to cardiovascular complications. Although patients with CKD have a higher burden of cardiovascular disease, the relationship between AGEs and cardiovascular disease in patients with CKD is not fully characterized. In this paper, we review the various deleterious effects of AGEs in CKD that lead to cardiovascular complications and the role of these AGEs in diabetic nephropathy. We also discuss potential pharmacologic approaches to circumvent these deleterious effects by reducing exogenous and endogenous sources of AGEs, increasing the breakdown of existing AGEs, or inhibiting AGE-induced inflammation. Finally, we speculate on preventive and therapeutic strategies that focus on the AGE-RAGE axis to prevent vascular complications in patients with CKD.

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“…Therefore, during CFPD with a high dialysate flow rate, an effective osmotic gradient can be maintained with very low glucose concentrations (104). Additionally, the online preparation of a bicarbonate solution using hemodialysis methodology provides a neutral-pH low-GDP PD fluid (105). At present, there are no reports of patients maintained at home on CFPD.…”

Section: Strategies To Reduce Glucose-related Toxicitymentioning

confidence: 99%

Impact of Glucose in Peritoneal Dialysis: Saint or Sinner?

Sitter

Sauter

2005

Perit Dial Int

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Peritoneal dialysis (PD) solutions using glucose as osmotic agent have been used for more than two decades as effective treatment for patients with end-stage renal disease. Although alternative osmotic agents such as amino acids and macromolecular solutions, including polypeptides and glucose polymers, are now available, glucose is still the most widely used osmotic agent in PD. It has been shown to be safe, effective, readily metabolized, and inexpensive. On the other hand, it is widely assumed that exposure of the peritoneal membrane to high glucose concentrations contributes to both structural and functional changes in the dialyzed peritoneal membrane. As in diabetes, glucose, either directly or indirectly through the generation of glucose degradation products or the formation of advanced glycation end products, may contribute to peritoneal membrane failure. Although efforts to reduce glucose toxicity have been made for years, only a few suggestions, such as dual-bag systems with bicarbonate as buffer system, have found broader acceptance. Recently, some interesting new approaches to the problem of glucose-related toxicity have been made, but further investigations will be necessary before they can be used clinically. This review will focus on adverse effects of glucose in PD solutions and summarize different aspects of glucotoxicity and potential therapeutic interventions.

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Continuous Flow Peritoneal Dialysis: Solution Formulation and Biocompatibility

Cited by 12 publications

References 40 publications

NFκB in the Development of Endothelial Activation and Damage in Uremia: An In Vitro Approach

NFκB in the Development of Endothelial Activation and Damage in Uremia: An In Vitro Approach

Uremic Toxicity of Advanced Glycation End Products in CKD

Impact of Glucose in Peritoneal Dialysis: Saint or Sinner?

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