Blood Microbiome Profile in CKD

Shah, Neal; Allegretti, Andrew S.; Nigwekar, Sagar U.; Kalim, Sahir; Zhao, Sophia; Lelouvier, Benjamin; Servant, Florence; Serena, Gloria; Thadhani, Ravi; Raj, Dominic S.; Fasano, Alessio

doi:10.2215/cjn.12161018

Cited by 96 publications

(106 citation statements)

References 51 publications

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“…High plasmatic levels of tryptophan metabolites like IAA in stage V non-HD and HD patients could activate aryl hydrocarbon receptors which regulate local IL-22 production for intestinal homeostasis [28] resulting in gut barrier protection. Interestingly, a recent study evaluated blood microbiome in non-diabetic CKD patients using 16S PCR: quantitative circulating 16S rDNA did not differ between CKD patients and controls [29] supporting the fact that bacterial translocation is not increased in non-diabetic CKD patients. Of course, we also can not eliminate a lack of effect and a falsely unchanged rate of bacterial translocation, due to the low number of patients in this pilot study.…”

Section: Discussionmentioning

confidence: 87%

Factors of microinflammation in non-diabetic chronic kidney disease: a pilot study

et al. 2020

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Background: The relationships between digestive bacterial translocation, uremic toxins, oxidative stress and microinflammation in a population of chronic kidney disease (CKD) patients without metabolic nor inflammatory disease are unknown. Methods: Bacterial translocation, uremic toxins, oxidative stress, and inflammation were assessed by measuring plasma levels of 16S ribosomal DNA (16S rDNA), p-cresyl sulfate (PCS), indoxyl sulfate (IS), indole acetic acid (IAA), F2-isoprostanes, hsCRP and receptor I of TNFα (RITNFα) in patients without metabolic nor inflammatory disease. 44 patients with CKD from stage IIIB to V and 14 controls with normal kidney function were included from the nephrology outpatients. 11 patients under hemodialysis (HD) were also included. Correlations between each factor and microinflammation markers were studied.Results: 16S rDNA levels were not increased in CKD patients compared to controls but were decreased in HD compared to non-HD stage V patients (4.7 (3.9-5.3) vs 8.6 (5.9-9.7) copies/μl, p = 0.002). IS, PCS and IAA levels increased in HD compared to controls (106.3 (73.3-130.4) vs 3.17 (2.4-5.1) μmol/l, p < 0.0001 for IS; 174.2 (125-227.5) vs 23.7 (13.9-52.6) μmol/l, p = 0.006 for PCS; and 3.7 (2.6-4.6) vs 1.3 (1.0-1.9) μmol/l, p = 0.0002 for IAA). Urea increased in non-HD stage V patients compared to controls (27.6 (22.7-30.9) vs 5.4 (4.8-6.4) mmol/l, p < 0.0001) and was similar in HD and in non-HD stage V (19.3 (14.0-24.0) vs 27.6 (22.7-30.9) mmol/l, p = 0.7). RITNFα levels increased in HD patients compared to controls (12.6 (9.6-13.3) vs 1.1 (1.0-1.4) ng/ml, p < 0.0001); hsCRP levels increased in non-HD stage V patients compared to controls (2.9 (1.4-8.5) vs 0.8 (0.5-1.7) mg/l, p = 0.01) and remained stable in HD patients (2.9 (1.4-8.5) vs 5.1 (0.9-11.5) mg/l, p = 1). F2-isoprostanes did not differ in CKD patients compared to controls. Among uremic toxins, IS and urea were correlated to RITNFα (r = 0.8, p < 0.0001 for both). PCS, IS and urea were higher in patients with hsCRP≧5 mg/l (p = 0.01, 0.04 and 0.001 respectively). 16S rDNA, F2-isoprostanes were not correlated to microinflammation markers in our study. Conclusions:In CKD patients without any associated metabolic nor inflammatory disease, only PCS, IS, and urea were correlated with microinflammation. Bacterial translocation was decreased in patients under HD and was not correlated to microinflammation.

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Section: Discussionmentioning

confidence: 87%

Factors of microinflammation in non-diabetic chronic kidney disease: a pilot study

et al. 2020

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“…76 However, more intensive chronic maintenance haemodialysis in patients with end-stage renal disease has not provided substantial reductions in the plasma levels of colon-derived uraemic solutes. 79 Whether the observed changes in the blood microbiome profile in CKD originate from the colon microbiome is unclear. 79 Whether the observed changes in the blood microbiome profile in CKD originate from the colon microbiome is unclear.…”

Section: Aki and Liver/intestine Dysfunctionmentioning

confidence: 99%

“…77,78 Also, variations in the blood microbiome profile have been described in patients with CKD compared with healthy subjects. 79 Whether the observed changes in the blood microbiome profile in CKD originate from the colon microbiome is unclear. Nevertheless, changes in gut microbiome have been linked to liver injury and the progression of CKD and a potential increase in cardiovascular risk.…”

Section: Aki and Liver/intestine Dysfunctionmentioning

confidence: 99%

Distant organ dysfunction in acute kidney injury

2019

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Acute kidney injury (AKI) is a common complication in critically ill patients and it is associated with increased morbidity and mortality. Epidemiological and clinical data show that AKI is linked to a wide range of distant organ injuries, with the lungs, heart, liver, and intestines representing the most clinically relevant affected organs. This distant organ injury during AKI predisposes patients to progression to multiple organ dysfunction syndrome and ultimately, death. The strongest direct evidence of distant organ injury occurring in AKI has been obtained from animal models. The identified mechanisms include systemic inflammatory changes, oxidative stress, increases in leucocyte trafficking and the activation of proapoptotic pathways.Understanding the pathways driving AKI-induced distal organ injury are critical for the development and refinement of therapies for the prevention and attenuation of AKI-related morbidity and mortality. The purpose of this review is to summarize both clinical and preclinical studies of AKI and its role in distant organ injury.

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“…However, through use of culture-independent methods, evidence has emerged regarding the healthy human blood microbiome (5). The signature of the blood microbiome has provided insight into diseases such as schizophrenia (6), type 2 diabetes (7,8), chronic kidney disease (9) and liver fibrosis (10), and may provide a link to the microbiome in other tissues and diseases.…”

Section: Introductionmentioning

confidence: 99%

Peripheral blood microbial signatures in COPD

Morrow

Castaldi

Chase

et al. 2020

Preprint

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Background:The human microbiome has a role in the development of human diseases. Individual microbiome profiles are highly personalized, though many species are shared. Understanding the relationship between the human microbiome and disease may inform future individualized treatments.Specifically, the blood microbiome, once believed sterile, may be a surrogate for some lung and gut microbial characteristics. We sought associations between the blood microbiome and lung-relevant host factors.Methods: Based on reads not mapped to the human genome, we detected microbial nucleic acid signatures in peripheral blood RNA-sequencing for 2,590 current and former smokers with and without chronic obstructive pulmonary disease (COPD) from the COPDGene study. We used the GATK microbial pipeline PathSeq to infer microbial profiles. We tested associations between the inferred profiles and lung disease relevant phenotypes and examined links to host gene expression pathways. Results:The four phyla with highest abundance across all subjects were Proteobacteria, Actinobacteria, Firmicutes and Bacteroidetes. We observed associations between exacerbation phenotypes and the relative abundance of Staphylococcus, Acidovorax and Cupriavidus. The genus Flavobacterium was associated with emphysema and change in emphysema. Our host-microbiome interaction analysis revealed clustering of genera associated with emphysema, systemic inflammation, airway remodeling and exacerbations, through links to lung-relevant host pathways. Conclusions:This study is the first to identify a bacterial microbiome signature in the peripheral blood of current and former smokers. Understanding the relationships between the systemic microbial populations and lung disease severity may inform novel interventions and aid in the understanding of exacerbation phenotypes. Abstract word count: 246 COPD Foundation FundingCOPDGene is also supported by the COPD Foundation through contributions made to an Industry

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Blood Microbiome Profile in CKD

Cited by 96 publications

References 51 publications

Factors of microinflammation in non-diabetic chronic kidney disease: a pilot study

Factors of microinflammation in non-diabetic chronic kidney disease: a pilot study

Distant organ dysfunction in acute kidney injury

Peripheral blood microbial signatures in COPD

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