A Renal Clinician's Guide to the Gut Microbiota

Snelson, Matthew; Biruete, Annabel; McFarlane, Catherine; Campbell, Katrina L.

doi:10.1053/j.jrn.2019.11.002

Cited by 25 publications

(17 citation statements)

References 133 publications

(144 reference statements)

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“…UTs are usually produced through the metabolism of amino acids by intestinal microbiota microbiota, and accumulated UTs can change the composition of intestinal microbiota. Increasing evidence shows that intestinal microbiota plays a crucial role in the development of CKD [51]. Therefore, the current methods of reducing UTs through diet control and supplement therapy include reducing protein intake through a low-protein or plantbased diet [52] and supplementing probiotics, prebiotics, and synbiotics to change the composition of intestinal microbiota; some supplements could exert anti-inflammatory and antioxidative effects [53].…”

Section: Diet Control and Diet Supplementsmentioning

confidence: 99%

The Therapeutic Strategies for Uremic Toxins Control in Chronic Kidney Disease

Wei

et al. 2021

Toxins

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Uremic toxins (UTs) are mainly produced by protein metabolized by the intestinal microbiota and converted in the liver or by mitochondria or other enzymes. The accumulation of UTs can damage the intestinal barrier integrity and cause vascular damage and progressive kidney damage. Together, these factors lead to metabolic imbalances, which in turn increase oxidative stress and inflammation and then produce uremia that affects many organs and causes diseases including renal fibrosis, vascular disease, and renal osteodystrophy. This article is based on the theory of the intestinal–renal axis, from bench to bedside, and it discusses nonextracorporeal therapies for UTs, which are classified into three categories: medication, diet and supplement therapy, and complementary and alternative medicine (CAM) and other therapies. The effects of medications such as AST-120 and meclofenamate are described. Diet and supplement therapies include plant-based diet, very low-protein diet, probiotics, prebiotics, synbiotics, and nutraceuticals. The research status of Chinese herbal medicine is discussed for CAM and other therapies. This review can provide some treatment recommendations for the reduction of UTs in patients with chronic kidney disease.

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Section: Diet Control and Diet Supplementsmentioning

confidence: 99%

The Therapeutic Strategies for Uremic Toxins Control in Chronic Kidney Disease

Wei

et al. 2021

Toxins

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“…The uremic toxins, indoxyl sulfate (IS) and p-cresyl sulfate (PCS), have increasingly been associated with accelerated kidney disease progression and cardiovascular morbidity and mortality [3][4][5]. These toxins are produced through the metabolism of the dietary amino acids, tryptophan (IS) and tyrosine (PCS), respectively, by the gut microbiota [6]. Both IS and PCS are predominantly bound to plasma proteins, such as albumin, and rely on kidney excretion.…”

Section: Introductionmentioning

confidence: 99%

Synbiotics Easing Renal Failure by Improving Gut Microbiology II (SYNERGY II): A Feasibility Randomized Controlled Trial

et al. 2021

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Synbiotics have emerged as a therapeutic strategy for modulating the gut microbiome and targeting novel cardiovascular risk factors, including uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate (PCS). This study aims to evaluate the feasibility of a trial of long-term synbiotic supplementation in adults with stage 3–4 chronic kidney disease (CKD). Adult participants with CKD and estimated glomerular filtration rate (eGFR) of 15–60 mL/min/1.73 m2) were recruited between April 2017 and August 2018 to a feasibility, double-blind, placebo-controlled, randomized trial of synbiotic therapy or matched identical placebo for 12 months. The primary outcomes were recruitment and retention rates as well as acceptability of the intervention. Secondary outcomes were treatment adherence and dietary intake. Exploratory outcomes were evaluation of the cardiovascular structure and function, serum IS and PCS, stool microbiota profile, kidney function, blood pressure, and lipid profile. Of 166 potentially eligible patients, 68 (41%) were recruited into the trial (synbiotic n = 35, placebo n = 33). Synbiotic and placebo groups had acceptable and comparable 12-month retention rates (80% versus 85%, respectively, p = 0.60). Synbiotic supplementation altered the stool microbiome with an enrichment of Bifidobacterium and Blautia spp., resulting in a 3.14 mL/min/1.73 m2 (95% confidence interval (CI), −6.23 to −0.06 mL/min/1.73 m2, p < 0.01) reduction in eGFR and a 20.8 µmol/L (95% CI, 2.97 to 38.5 µmol/L, p < 0.01) increase in serum creatinine concentration. No between-group differences were observed in any of the other secondary or exploratory outcomes. Long-term synbiotic supplementation was feasible and acceptable to patients with CKD, and it modified the gastrointestinal microbiome. However, the reduction in kidney function with synbiotics warrants further investigation.

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“…[ 57 ] Future studies would benefit from the use of shotgun metagenomics, to enhance the resolution of bacterial species identified and metatranscriptomics to provide greater insight into the functional impact of the microbiota. [ 58 ] Whilst the current study observed that a high protein diet was associated with renal injury, there was only a trend towards concomitant renal fibrosis. Previous animal studies that have utilized rats [ 26,27 ] and pigs [ 33 ] have observed that high protein diets are associated with an increase in glomerulosclerosis.…”

Section: Discussionmentioning

confidence: 58%

Long Term High Protein Diet Feeding Alters the Microbiome and Increases Intestinal Permeability, Systemic Inflammation and Kidney Injury in Mice

Snelson

Clarke

Nguyen

et al. 2021

Molecular Nutrition Food Res

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This study evaluates the effects of a chronic high protein diet (HPD) on kidney injury, intestinal permeability and gut microbiota perturbations in a mouse model. Method and results: Mice are fed a diet containing either 20% or 52% energy from protein for 24 weeks; protein displaced an equivalent amount of wheat starch. The HPD does not alter glycemic control or body weight. The HPD induces kidney injury as evidenced by increase in albuminuria, urinary kidney injury molecule-1, blood urea nitrogen, urinary isoprostanes and renal cortical NF-B p65 gene expression. HPD decreases intestinal occludin gene expression, increases plasma endotoxin and plasma monocyte chemoattractant protein-1, indicating intestinal leakiness and systemic inflammation. Cecal microbial analysis reveals that HPD feeding does not alter alpha diversity; however, it does alter beta diversity, indicating an altered microbial community structure with HPD feeding. Predicted metagenome pathway analysis demonstrates a reduction in branched-chain amino acid synthesis and an increase of the urea cycle with consumption of a HPD. Conclusion: These results demonstrate that long term HPD consumption in mice causes albuminuria, systemic inflammation, increase in gastrointestinal permeability and is associated with gut microbiome remodeling with an increase in the urea cycle pathway, which may contribute to renal injury.

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A Renal Clinician's Guide to the Gut Microbiota

Cited by 25 publications

References 133 publications

The Therapeutic Strategies for Uremic Toxins Control in Chronic Kidney Disease

The Therapeutic Strategies for Uremic Toxins Control in Chronic Kidney Disease

Synbiotics Easing Renal Failure by Improving Gut Microbiology II (SYNERGY II): A Feasibility Randomized Controlled Trial

Long Term High Protein Diet Feeding Alters the Microbiome and Increases Intestinal Permeability, Systemic Inflammation and Kidney Injury in Mice

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