New Tricks for Old Friends: Treating Gut Microbiota of Patients With CKD

Mafra, Denise; Kalantar-Zadeh, Kamyar; Moore, Linda W.

doi:10.1053/j.jrn.2021.07.002

Cited by 9 publications

(8 citation statements)

References 54 publications

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“…Moreover, such dietary habits have the potential to alter gut microbiota to result in a more favorable milieu. These alterations can result in less production of the proinflammatory uremic toxins and potentially ameliorate the outcome of COVID‐19 (12). Furthermore, other factors, including age (13) and pregnancy (14), may alter the microbiome milieu and can potentially affect COVID‐19 outcomes.…”

Section: Discussionmentioning

confidence: 99%

Gut microbiome and diet in populations with obesity: Role of the Na+/K+‐ATPase transporter signaling in severe COVID‐19

Khitan

Chin

Sodhi

et al. 2022

Obesity

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Objective The triad of obesity, a high‐protein diet from animal sources, and disturbed gut microbiota have been linked to poor clinical outcomes in patients with COVID‐19. In this report, the effect of oxidative stress resulting from the Na+/K+‐ATPase transporter signaling cascade is explored as a driver of this poor clinical outcome. Methods Protein–protein interactions with the SARS‐CoV‐2 proteome were identified from the interactome data for Na+/K+‐transporting ATPase subunit α‐1 (ATP1A1), epidermal growth factor receptor, and ERB‐B2 receptor tyrosine kinase 2, using the curated data from the BioGRID Database of Protein Interactions. Data for the gene expression pattern of inflammatory response were from the Gene Expression Omnibus database for cardiomyocytes post SARS‐CoV‐2 infection (number http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151879). Results The ATP1A1 subunit of the Na+/K+‐ATPase transporter is targeted by multiple SARS‐CoV‐2 proteins. Furthermore, receptor proteins associated with inflammatory response, including epidermal growth factor receptor and ERB‐B2 receptor tyrosine kinase 2 (which interact with ATP1A1), are also targeted by some SARS‐CoV‐2 proteins. This heightened interaction likely triggers a cytokine release that increases the severity of the viral infection in individuals with obesity. Conclusions The similarities between the effects of SARS‐CoV‐2 proteins and indoxyl sulphate on the Na+/K+‐ATPase transporter signaling cascade suggest the possibility of an augmentation of gene changes seen with COVID‐19 infection that can result in a hyperinduction of cytokine release in individuals with obesity.

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Section: Discussionmentioning

confidence: 99%

Gut microbiome and diet in populations with obesity: Role of the Na+/K+‐ATPase transporter signaling in severe COVID‐19

Khitan

Chin

Sodhi

et al. 2022

Obesity

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“…In 2019, the International Scientific Association for Probiotics and Prebiotics (ISAPP) updated the synbiotic definition as “a mixture comprising live microorganisms and substrate(s) selectively utilised by host microorganisms that confers a health benefit on the host” [ 100 ]. Thus, synbiotics have emerged as a potential therapeutic strategy to modulate the gut microbiota and, hence, decrease harmful metabolites, such as uremic toxins, related to uremic dysbiosis [ 2 ]. One of the first studies regarding the effects of synbiotics for patients with CKD observed that one packet of synbiotics three times a day for two weeks improved constipation and reduced p-CS serum levels in patients undergoing HD [ 101 ].…”

Section: Gut Microbiota Modulation and Effects On Residual Kidney Fun...mentioning

confidence: 99%

“…In general, these studies show reduced alpha diversity and an accumulation of uremic toxins generated by the gut microbiota, such as phenylacetylglutamine (PAGln), cinnamoylglycine, p-cresyl sulfate (p-CS), phenyl sulfate (PS), hippuric acid, indoxyl sulfate (IS), p-cresyl glucuronide, trimethylamine N-oxide (TMAO), indol acetic acid and phenylacetylglycine (PAGly). Moreover, studies have shown that levels of short-chain fatty acids (SCFA) produced by certain bacteria (Blautia, unidentified Ruminococcaceae and Parabacteroidies) with beneficial effects on health (anti-inflammatory responses, gut barrier modulation and reduction of bacterial translocation) are reduced because of limited SCFA-producing bacteria [1,2]. Deleterious effects, such as inflammation, oxidative stress, atherosclerosis Toxins 2023, 15, 499 2 of 20 and renal fibrosis with decreased kidney function, have been reported due to dysbiosis [3,4].…”

Section: Introductionmentioning

confidence: 99%

Gut Microbiota Interventions to Retain Residual Kidney Function

Mafra

Kemp

Borges

et al. 2023

Toxins

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Residual kidney function for patients with chronic kidney disease (CKD) is associated with better quality of life and outcome; thus, strategies should be implemented to preserve kidney function. Among the multiple causes that promote kidney damage, gut dysbiosis due to increased uremic toxin production and endotoxemia need attention. Several strategies have been proposed to modulate the gut microbiota in these patients, and diet has gained increasing attention in recent years since it is the primary driver of gut dysbiosis. In addition, medications and faecal transplantation may be valid strategies. Modifying gut microbiota composition may mitigate chronic kidney damage and preserve residual kidney function. Although various studies have shown the influential role of diet in modulating gut microbiota composition, the effects of this modulation on residual kidney function remain limited. This review discusses the role of gut microbiota metabolism on residual kidney function and vice versa and how we could preserve the residual kidney function by modulating the gut microbiota balance.

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“…Gut dysbiosis is both a quantitative and qualitative alteration in the composition and metabolic profiles of the gut microbiome. Increasing evidence has confirmed gut dysbiosis occurs at the onset of CKD, including in the development of CKD and progression to endstage kidney disease (ESKD) [47][48][49]. Recent pre-clinical and clinical studies exploring gut microbiota features in CKD are summarized in Table 1, focusing on the relative abundance of primary bacterial groups, such as Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, Fusobacteria, and Verrucomicrobia compared to controls.…”

Section: Evidence Of Gut Microbiota Dysbiosis In Ckdmentioning

confidence: 99%

Faecal Microbiota Transplantation and Chronic Kidney Disease

et al. 2022

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Faecal microbiota transplantation (FMT) has attracted increasing attention as an intervention in many clinical conditions, including autoimmune, enteroendocrine, gastroenterological, and neurological diseases. For years, FMT has been an effective second-line treatment for Clostridium difficile infection (CDI) with beneficial outcomes. FMT is also promising in improving bowel diseases, such as ulcerative colitis (UC). Pre-clinical and clinical studies suggest that this microbiota-based intervention may influence the development and progression of chronic kidney disease (CKD) via modifying a dysregulated gut–kidney axis. Despite the high morbidity and mortality due to CKD, there are limited options for treatment until end-stage kidney disease occurs, which results in death, dialysis, or kidney transplantation. This imposes a significant financial and health burden on the individual, their families and careers, and the health system. Recent studies have suggested that strategies to reverse gut dysbiosis using FMT are a promising therapy in CKD. This review summarises the preclinical and clinical evidence and postulates the potential therapeutic effect of FMT in the management of CKD.

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New Tricks for Old Friends: Treating Gut Microbiota of Patients With CKD

Cited by 9 publications

References 54 publications

Gut microbiome and diet in populations with obesity: Role of the Na+/K+‐ATPase transporter signaling in severe COVID‐19

Gut microbiome and diet in populations with obesity: Role of the Na+/K+‐ATPase transporter signaling in severe COVID‐19

Gut Microbiota Interventions to Retain Residual Kidney Function

Faecal Microbiota Transplantation and Chronic Kidney Disease

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