Specific Alterations in Gut Microbiota in Patients with Chronic Kidney Disease: An Updated Systematic Review

Specific Alterations in Gut Microbiota in Patients with Chronic Kidney Disease: An Updated Systematic Review

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Introduction

Gut dysbiosis may be involved in the pathophysiology of CKD and the relationship between the intestine and kidney is referred to as the ‘gut-kidney axis,’ in which the gut microbiota is an essential component. Gut dysbiosis is a condition in which the microbiota is abnormally abundant which can lead to immunological, metabolic, or endocrine issues. It may cause an imbalance in immunological responses and tolerance which may contribute to the initiation and progression of CKD.

Metabolites derived from gut microbiota, such as trimethylamine-N-oxide (TMAO), p-cresyl sulphate (PCS), indoxyl sulphate (IS), and phenylacetylglutamine (PAG), as well as fermentation products may contribute to declining kidney function and worsening cardiovascular diseases, whereas short-chain fatty acids (SCFAs), fermentation products of dietary fibre exert protective effects on the kidney (Fig 1.) This study performed a systematic review to analyze the bacterial diversity in patients with CKD.

Study Protocol

A total of 150 records were retrieved; 25, ranging from 2012 to 2020, were eligible for inclusion in our systematic review (Figure 2).

The 25 studies included 1436 patients with CKD and 918 healthy controls. Nine studies focused on ESRD; 12 focused on CKD ranging in severity from stage 1 to 5; and four focused on two specific pathological types of CKD: IgA nephropathy (IgAN) and DN. Seventeen studies were carried out in China, three in the US, two in Italy, and one in Austria, Brazil, and Netherlands.

Nineteen studies conducted full-scale analysis of the gut microbial profile, while six were limited to specific bacteria at the species level and mainly applied polymerase chain reaction (PCR) analysis. Patients in eight studies received renal replacement therapy including hemodialysis (n = 419), peritoneal dialysis (n = 68), or kidney transplantation (n = 20).

The study summarized the existing evidence describing the profile of gut microbiota in patients with CKD or ESRD with the aim of identifying specific microbial taxa that could contribute to disease pathogenesis. The progression could form the basis for new approaches to modulate gut dysbiosis to treat and prevent CKD. The alterations in gut microbial profiles in patients with CKD or ESRD were determined and are shown in Table 1.

Conclusion

The current study supports the increased abundance of phylum Proteobacteria and Fusobacteria, genus Escherichia Shigella, Desulfovibrio, and Streptococcus, while lower abundance of genus Roseburia, Faecalibacterium, Pyramidobacter, Prevotellaceae UCG-001, and Prevotella 9 in patients with CKD; and increased abundance of phylum Proteobacteria, and genus Streptococcus and Fusobacterium, while lower abundance of Prevotella, Coprococcus, Megamonas, and Faecalibacterium in patients with ESRD.

Furthermore, advanced CKD patients had greater TMAO and PCS concentrations but lower SCFA concentrations. However, due to the variability of the available data, the features of the gut microbiota in individuals with CKD were not established. Further research should use high-throughput sequencing technology and comprehensive reporting to gain a better understanding of the gut microbiota, which could lead to a better understanding of the underlying mechanisms of how the gut microbiota interacts with CKD and its potential implications in CKD treatment and prevention.

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