Abstract

Indoxyl sulphate (IS) and p-cresyl sulphate (PCS) are two protein bound uraemic toxins accumulated in chronic kidney disease (CKD) and associated with adverse outcomes. The purpose of this study isto evaluate the effect of the new activated charcoal, CharXgen, on renal function protection and lowering serum uraemic toxins in CKD animal model. The physical character of CharXgen was analyzed before and after activation procedure by Scanning Electron Microscope (SEM) and X-ray diffractometer (XRD). The effect of CharXgen on biochemistry and lowering uremic toxins was evaluated by in vitro binding assay and CKD animal model. CharXgen have high interior surface area analyzed by SEM and XRD and have been produced from local bamboo after an activation process. CharXgen was able to effectively absorb IS, p-cresol and phosphate in an in vitro gastrointestinal tract simulation study. The animal study showed that CharXgen did not cause intestine blackening. Serum albuminand liver function did not change after feeding with CharXgen. Moreover, renal function was improved in CKD rats fed with CharXgen as compared to the CKD group, and there were no significant differences in the CKD and the CKD + AST-120 groups. Serum IS and PCS were higher in the CKD group and lower in rats treated with CharXgen and AST-120. In rats treated with CharXgen, Fibroblast growth factor 23 was significantly decreased as compared to the CKD group. This change cannot be found in rats fed with AST-120.It indicates that CharXgen is a new safe and non-toxic activated charcoal having potential in attenuating renal function deterioration and lowering protein-bound uraemic toxins. Whether the introduction of this new charcoal could further have renal protection in CKD patients will need to be investigated further.

Highlights

  • The risk of cardiovascular disease (CVD) is markedly increased in patients with chronic kidney disease (CKD) [1], especially in those with end stage renal disease (ESRD) [2,3]

  • Uraemic solutes, including indoxyl sulphate (IS) and p-cresol sulphate (PCS), which are two protein-bound uraemic toxins originating from the intestinal tract following the metabolism of aromatic amino acids by the intestinal flora, inhibit endothelial proliferation, which may contribute to endothelial cell dysfunction [10,11]

  • Serum levels of IS and PCS were lower in rats fed with CharXgen or AST-120 as compared to CKD rats. These results showed that the binding capacity of CharXgen to protein-bound uraemic toxins was not inferior to AST-120

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Summary

Introduction

The risk of cardiovascular disease (CVD) is markedly increased in patients with chronic kidney disease (CKD) [1], especially in those with end stage renal disease (ESRD) [2,3]. Evidence has supported and emphasized the concept of non-traditional risk factors [6,7,8,9], which include accumulation of uraemic toxins, with a decline in renal function. Fibroblast growth factor 23 (FGF23), a phosphaturic factor secreted from bone, increased in renal failure [23]. Evidence has demonstrated that FGF 23 is not just a major regulator in mineral-bone disorder but rather a factor responsible for cardiovascular morbidity and mortality in patients with CKD [25]

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