Division of Renal Diseases and Hypertension, The George Washington University, Washington DC.
J Am Soc Nephrol. 2014 Apr;25(4):657-70. doi: 10.1681/ASN.2013080905. Epub 2013 Nov 14.
The human gut harbors >100 trillion microbial cells, which influence the nutrition, metabolism, physiology, and immune function of the host. Here, we review the quantitative and qualitative changes in gut microbiota of patients with CKD that lead to disturbance of this symbiotic relationship, how this may contribute to the progression of CKD, and targeted interventions to re-establish symbiosis. Endotoxin derived from gut bacteria incites a powerful inflammatory response in the host organism. Furthermore, protein fermentation by gut microbiota generates myriad toxic metabolites, including p-cresol and indoxyl sulfate. Disruption of gut barrier function in CKD allows translocation of endotoxin and bacterial metabolites to the systemic circulation, which contributes to uremic toxicity, inflammation, progression of CKD, and associated cardiovascular disease. Several targeted interventions that aim to re-establish intestinal symbiosis, neutralize bacterial endotoxins, or adsorb gut-derived uremic toxins have been developed. Indeed, animal and human studies suggest that prebiotics and probiotics may have therapeutic roles in maintaining a metabolically-balanced gut microbiota and reducing progression of CKD and uremia-associated complications. We propose that further research should focus on using this highly efficient metabolic machinery to alleviate uremic symptoms.
人类肠道中栖息着超过 1000 万亿个微生物细胞,这些微生物会影响宿主的营养、代谢、生理和免疫功能。在这里,我们综述了 CKD 患者肠道微生物群的数量和质量变化,这些变化导致了这种共生关系的紊乱,以及这种变化如何促进 CKD 的进展,和重新建立共生关系的靶向干预措施。来自肠道细菌的内毒素会在宿主中引发强烈的炎症反应。此外,肠道微生物群的蛋白质发酵会产生无数有毒代谢物,包括对甲酚和吲哚硫酸酯。CKD 中肠道屏障功能的破坏会导致内毒素和细菌代谢物向全身循环转移,从而导致尿毒症毒性、炎症、CKD 进展和相关心血管疾病。已经开发了几种靶向干预措施,旨在重新建立肠道共生关系、中和细菌内毒素或吸附肠道来源的尿毒症毒素。事实上,动物和人体研究表明,益生元和益生菌可能在维持代谢平衡的肠道微生物群和减少 CKD 进展和尿毒症相关并发症方面具有治疗作用。我们提出,应进一步研究利用这种高效代谢机制来缓解尿毒症症状。