Gut bacterial translocation is associated with microinflammation in end-stage renal disease patients
ABSTRACT Aim: To investigate whether gut bacteria translocation occurs in end‐stage renal disease patients and contributes to microinflammation in end‐stage renal disease (ESRD). Methods: The subjects were divided into two groups: nondialysed ESRD patients (n = 30) and healthy controls (n = 10). B...
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Published in | Nephrology (Carlton, Vic.) Vol. 17; no. 8; pp. 733 - 738 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Melbourne, Australia
Blackwell Publishing Asia
01.11.2012
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Subjects | |
Online Access | Get full text |
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Summary: | ABSTRACT
Aim: To investigate whether gut bacteria translocation occurs in end‐stage renal disease patients and contributes to microinflammation in end‐stage renal disease (ESRD).
Methods: The subjects were divided into two groups: nondialysed ESRD patients (n = 30) and healthy controls (n = 10). Blood samples from all participants were subjected to bacterial 16S ribosomal DNA amplification and DNA pyrosequencing to determine the presence of bacteria, and the alteration of gut microbiomes were examined with the same methods. High‐sensitive C‐reactive protein and interleukin‐6 were detected. Plasma D‐lactate was tested for gut permeability.
Results: Bacterial DNAs were detected in the blood of 20% (6/30) of the ESRD patients. All the observed genera in blood (Klebsiella spp, Proteus spp, Escherichia spp, Enterobacter spp, and Pseudomonas spp) were overgrown in the guts of the ESRD patients. Plasma D‐lactate, High‐sensitive C‐reactive protein, and interleukin‐6 levels were significantly higher in patients with bacterial DNA than those without. The control group showed the same results as that of patients without bacterial DNA.
Conclusion: Bacterial translocation occurs in ESRD patients and is associated with microinflammation in end stage renal disease.
Wang et al. evaluated the bacterial translocation in the intestinal tract in non‐dialysed ESRD patients and its contribution to micoinflammation in the patient population. |
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Bibliography: | istex:DC4253BDD43F9E4357CD2064E194A6C53E952899 ark:/67375/WNG-PGBS2DX0-7 ArticleID:NEP1647 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 1320-5358 1440-1797 1440-1797 |
DOI: | 10.1111/j.1440-1797.2012.01647.x |