Abstract
Peritoneal dialysis (PD) is an important, if underprescribed, modality for the treatment of patients with end-stage kidney disease. Among the barriers to its wider use are the deleterious effects of currently commercially available glucose-based PD solutions on the morphological integrity and function of the peritoneal membrane due to fibrosis. This is primarily driven by hyperglycaemia due to its effects, through multiple cytokine and transcription factor signalling—and their metabolic sequelae—on the synthesis of collagen and other extracellular membrane components. In this review, we outline these interactions and explore how novel PD solution formulations are aimed at utilizing this knowledge to minimise the complications associated with fibrosis, while maintaining adequate rates of ultrafiltration across the peritoneal membrane and preservation of patient urinary volumes. We discuss the development of a new generation of reduced-glucose PD solutions that employ a variety of osmotically active constituents and highlight the biochemical rationale underlying optimization of oxidative metabolism within the peritoneal membrane. They are aimed at achieving optimal clinical outcomes and improving the whole-body metabolic profile of patients, particularly those who are glucose-intolerant, insulin-resistant, or diabetic, and for whom daily exposure to high doses of glucose is contraindicated.
Highlights
The increasing worldwide number of patients suffering from end-stage kidney failure (ESKF) who require a chronic renal replacement therapy (RRT) represents a significant economic burden on health systems globally [1]
We review established and novel approaches aimed at improving the biocompatibility of Peritoneal dialysis (PD) solutions, and the viability of the technique and optimization of clinical outcomes
It is noteworthy that Si et al have recently shown that by attenuating high glycolytic fluxes with 2-deoxyglucose, they could remarkably reduce TGF-beta1-induced profibrotic cellular phenotype in peritoneal mesothelial cells and peritoneal fibrosis in mice induced by a high peritoneal glucose load similar to that used in peritoneal dialysis [55]
Summary
The increasing worldwide number of patients suffering from end-stage kidney failure (ESKF) who require a chronic renal replacement therapy (RRT) represents a significant economic burden on health systems globally [1]. Among RRTs, peritoneal dialysis (PD) represents a well-established, cost-effective modality that can be delivered at home It is based on the depuration of uremic blood through exchanges between peritoneal capillaries and a solution infused into the peritoneal cavity via an implanted catheter (dialytic exchange). The dialytic exchange can be performed manually (continuous ambulatory PD; CAPD) or by employing fresh PD; dialysate is usually reinfused into the a cycler ESKF patients, it is addition, it preserves residual function betterfor and removes solutes and fluid still underprescribed [1]. This may be explained byPD major in PD efficiency and more gradually [2]. UF failure and a loss eventually leading to UFtofailure [8]. [8]
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