Gut Microbiome Profiling Uncovers a Lower Abundance of Butyricicoccus in Advanced Stages of Chronic Kidney Disease

Abstract

Chronic kidney disease (CKD) is characterized by the accumulation of uremic toxins which exert deleterious effects on various organ systems. Several of these uremic toxins originate from the bacterial metabolization of aromatic amino acids in the colon. This study assessed whether the gut microbial composition varies among patients in different stages of CKD. Uremic metabolites were quantified by UPLC/fluorescence detection and microbial profiling by 16S rRNA amplicon sequencing. Gut microbial profiles of CKD patients were compared among stages 1–2, stage 3 and stages 4–5. Although a substantial inter-individual difference in abundance of the top 15 genera was observed, no significant difference was observed between groups. Bristol stool scale (BSS) correlated negatively with p-cresyl sulfate and hippuric acid levels, irrespective of the intake of laxatives. Butyricicoccus, a genus with butyrate-generating properties, was decreased in abundance in advanced stages of CKD compared to the earlier stages (p = 0.043). In conclusion, in this cross-sectional study no gradual differences in the gut microbial profile over the different stages of CKD were observed. However, the decrease in the abundance of Butyricicoccus genus with loss of kidney function stresses the need for more in-depth functional exploration of the gut microbiome in CKD patients not on dialysis.

Berberine ameliorates chronic kidney disease through inhibiting the production of gut-derived uremic toxins in the gut microbiota

“…It was observed that g_Butyricicoccus , g_Proteus , g_Lactococcus , g_Eubacterium_oxidoreducens_group , g_Lachnospiraceae_NK4A136_group, g_Family_XIII_UCG-001, g_Shuttleworthia , g_Anaerovorax, g_Streptococcus, g_Lachnospiraceae_UCG-006, g_Lachnospiraceae_UCG-008 , g_Eubacterium_siraeum_group, g_Colidextribacter, and g_Roseburia were negatively correlated with plasma creatinine, plasma TMAO, plasma p -cresol sulfate and plasma indoxyl sulfate. Of note, a large number of butyric acid-producing bacteria were found among these strains, including g_Butyricicoccus 47 , g_Lachnospiraceae_NK4A136_group 48 , g_Lachnospiraceae_UCG-006 49 , g_Lachnospiraceae_UCG-008 49 and g_Roseburia 50 . And compared with the Model group, BBR increased the abundance of abovementioned genera ( Fig.…”

Prevalence and Severity of Lower Gastrointestinal Symptoms amongst Non-Dialysis Chronic Kidney Disease Patients: A Systematic Review and Meta-Analysis

“…The relationships between stool consistency and other data are shown in Table S20 . Briefly, two research teams found that the harder the stool consistency, the higher the concentration of some uremic solutes such as p -cresyl sulfate and hippuric acid in serum/plasma [ 33 , 40 , 48 ]. Both Meade et al and Ramos et al reported no associations between dietary parameters and stool consistency [ 40 , 47 ].…”

“…Previous studies have linked several lower GI symptoms with dysbiosis in the general population [ 87 , 88 ], so how it is related to the dysbiosis observed in CKD must be revealed [ 89 ]. Surprisingly, none of the studies to date have included patient GI symptomatology in the assessment of dysbiosis in CKD, with one exception that found that variation of the microbial composition was correlated with stool consistency [ 48 ].…”

Causal effects between gut microbiota and IgA nephropathy: a bidirectional Mendelian randomization study

“…Besides the mechanisms of butyrate affecting IgAN mentioned previously, there are several pathways through which butyrate can produce cellular effects to influence the physiological functions of the kidney. (I) G protein-coupled receptor (GPCR) signaling pathway regulatory mechanism: studies ( Gryp et al., 2021 ) have revealed that butyrate can activate Gpr41 (free fatty acid receptor 3, FFAR3) and Gpr43 (free fatty acid receptor 4, FFAR4), which are expressed in both the kidney and renal arteries, thereby affecting the metabolic and immune responses of the kidney ( Pluznick et al., 2013 ; Han et al., 2022 ). In addition, butyrate inhibited the proliferation of glomerular thylakoid cells induced by several factors via GPCR and can also reverse the production of reactive oxygen species (ROS) and malondialdehyde (MDA) ( Takeyasu et al., 1988 ).…”