The gut-kidney axis.

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...

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Publicado en:Pediatric Nephrology Vol. 32; no. 11; pp. 2005 - 2015
Autores principales: Evenepoel, Pieter, Poesen, Ruben, Meijers, Björn
Formato: pictorial review tables/charts Journal Article
Publicado: Springer Nature Nov2017
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Nov2017
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      pub: Springer Nature
      place: New York, New York
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        atl: The gut-kidney axis.
      aug:
        au:
          Evenepoel, Pieter
          Poesen, Ruben
          Meijers, Björn
      sug:
        subj:
          Gut Microbiota Metabolism
          Uremia Metabolism
          Renal Insufficiency, Chronic Metabolism
          Uremia Etiology
          Kidney Metabolism
          Renal Insufficiency, Chronic Etiology
          Renal Insufficiency, Chronic Physiopathology
          Uremia Complications
          Gut Microbiota Pathology
          Indoles
          Bacterial Toxins
          Endotoxins
          Proteins Metabolism
          Fermentation
          Phenols Metabolism
          Choline Metabolism
          Carnitine Metabolism
      ab: 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.
      pubtype: Academic Journal
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    language: English
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