Gut microbiome in chronic kidney disease
| Autor: | Maria R. Wing, Dominic S. Raj, Samir S. Patel, Ali Ramezani |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Gastrointestinal tract biology Gastrointestinal Microbiome 030232 urology & nephrology Inflammation General Medicine Disease Gut flora medicine.disease biology.organism_classification digestive system Microbiology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Immunology medicine Microbiome medicine.symptom Dysbiosis Kidney disease |
| Zdroj: | Experimental Physiology. 101:471-477 |
| ISSN: | 0958-0670 |
| Popis: | What is the topic of this review? This review addresses the contribution of the altered gut microbiome to uraemic syndrome, with specific reference to gut microbiome-derived uraemic toxins. It also discusses the potential treatment options to normalize the disturbed microbiome in chronic kidney disease (CKD). What advances does it highlight? This review highlights the importance of the gut-kidney connection and how the altered microbial landscape in the intestine contributes to dysmetabolism and inflammation in CKD. Recent findings linking gut-derived uraemic toxins to progression of CKD, cardiovascular disease and mortality are also discussed. Finally, we briefly explain targeted therapies that have been studied to restore intestinal symbiosis in CKD. The human intestine is now recognized as an important metabolic organ powered by gut microbiota. This review addresses the alteration in the gut microbiome in patients with chronic kidney disease (CKD) and its consequence. We describe the major uraemic toxins, p-cresol sulfate, indoxyl sulfate and trimethylamine N-oxide, which are produced by the gut microbiome, and how these metabolites contribute to progression of CKD and associated cardiovascular disease. Translocation of endotoxin from the gut into the systemic circulation contributes to inflammation in CKD. Targeting the gut microbiome to restore symbiosis may prove to be a potent strategy in reducing inflammation and production of these uraemic toxins. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text