We are analyzing https://link.springer.com/article/10.1007/s00467-016-3527-x.

Title:
The gut–kidney axis | Pediatric Nephrology
Description:
The host–gut microbiota interaction has been the focus of increasing interest in recent years. It has been determined that this complex interaction is not only essential to many aspects of normal “mammalian” physiology but that it may also contribute to a multitude of ailments, from the obvious case of inflammatory bowel disease to (complex) diseases residing in organs outside the gut. An increasing body of evidence indicates that crosstalk between host and microbiota is pathophysiologically relevant in patients with chronic kidney disease (CKD). Interactions are bidirectional; on the one hand, uremia affects both the composition and metabolism of the gut microbiota and, on the other hand, important uremic toxins originate from microbial metabolism. In addition, gut dysbiosis may induce a disruption of the epithelial barrier, ultimately resulting in increased exposure of the host to endotoxins. Due to dietary restrictions and gastrointestinal dysfunctions, microbial metabolism shifts to a predominantly proteolytic fermentation pattern in CKD. Indoxyl sulfate and p-cresyl sulfate, both end-products of protein fermentation, and trimethylamine-N-oxide, an end-product of microbial choline and carnitine metabolism, are prototypes of uremic toxins originating from microbial metabolism. The vascular and renal toxicity of these co-metabolites has been demonstrated extensively in experimental and clinical studies. These co-metabolites are an appealing target for adjuvant therapy in CKD. Treatment options include dietary therapy, prebiotics, probiotics and host and bacterial enzyme inhibitors. Final proof of the concept should come from randomized controlled and adequately powered intervention studies.
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Keywords {🔍}

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Topics {✒️}

host–gut microbiota interaction month download article/chapter protein-bound uraemic toxins metabolite-sensing receptors gpr43 protein-bound uremic toxins serum trimethylamine-n-oxide prebiotic oligofructose-enriched inulin real-time pcr analysis long-term dialysis patients end-stage renal disease alters microbial flora human gut microbiome microbiome–metabolome reveals apolipoprotein e-deficient mice full article pdf gut microbial enterotypes human microbiome project human microbiome enterotype inflammatory bowel disease trimethylamine-n-oxide human gut microbiota intestinal microbial metabolism microbial metabolism shifts chronic kidney disease intestinal microbiota metabolism retained microbial-human gut flora metabolism colonic microbial metabolism krishnamurthy vm p-cresol sulphate privacy choices/manage cookies p-cresyl sulphate aryl hydrocarbon receptor uremic toxins originating protein-bound solutes gut–kidney axis protein metabolite hypothesis inhibits cell senescence serum indoxyl sulphate meijers bk p-cresol-forming free p-cresol nuclear factor-kb tissue factor stability free serum concentrations university hospitals leuven european economic area jansson jk p-cresyl sulfate chronic renal failure

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         description:The host–gut microbiota interaction has been the focus of increasing interest in recent years. It has been determined that this complex interaction is not only essential to many aspects of normal “mammalian” physiology but that it may also contribute to a multitude of ailments, from the obvious case of inflammatory bowel disease to (complex) diseases residing in organs outside the gut. An increasing body of evidence indicates that crosstalk between host and microbiota is pathophysiologically relevant in patients with chronic kidney disease (CKD). Interactions are bidirectional; on the one hand, uremia affects both the composition and metabolism of the gut microbiota and, on the other hand, important uremic toxins originate from microbial metabolism. In addition, gut dysbiosis may induce a disruption of the epithelial barrier, ultimately resulting in increased exposure of the host to endotoxins. Due to dietary restrictions and gastrointestinal dysfunctions, microbial metabolism shifts to a predominantly proteolytic fermentation pattern in CKD. Indoxyl sulfate and p-cresyl sulfate, both end-products of protein fermentation, and trimethylamine-N-oxide, an end-product of microbial choline and carnitine metabolism, are prototypes of uremic toxins originating from microbial metabolism. The vascular and renal toxicity of these co-metabolites has been demonstrated extensively in experimental and clinical studies. These co-metabolites are an appealing target for adjuvant therapy in CKD. Treatment options include dietary therapy, prebiotics, probiotics and host and bacterial enzyme inhibitors. Final proof of the concept should come from randomized controlled and adequately powered intervention studies.
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         Nephrology
         Urology
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