scholarly journals Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Simona Mihai ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Ana-Maria Enciu ◽  
Lucian Albulescu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Gut Microbiota ◽  
Clinical Care ◽  
Low Grade ◽  
Public Health Burden ◽  
Inflammatory Status ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

Evidence from comparative genomic analyses indicating that Lactobacillus-mediated irritable bowel syndrome alleviation is mediated by the conjugated linoleic acid synthesis

2021 ◽  
Author(s):  
Yang Liu ◽  
Wei Xiao ◽  
Leilei Yu ◽  
Fengwei Tian ◽  
Gang Wang ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Linoleic Acid ◽  
Gut Microbiota ◽  
Acid Synthesis ◽  
Comparative Genomic ◽  
Low Grade ◽  
Genomic Analyses ◽  
Irritable Bowel ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

Irritable bowel syndrome (IBS) is a chronic intestinal disorder accompanied by low-grade inflammation, visceral hypersensitivity, and gut microbiota dysbiosis. Several studies have indicated that Lactobacillus supplementation can help to alleviate...

scholarly journals Inflammation in chronic kidney disease: sources, consequences and anti-inflammatory therapy.

2018 ◽  
Vol 96 (4) ◽  
pp. 314-320
Author(s):  
K. A. Aitbaev ◽  
Ilkhom T. Murkamilov ◽  
V. V. Fomin ◽  
J. A. Murkamilova ◽  
Z. R. Rayimzhanov ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Kidney Disease ◽  
Filtration Rate ◽  
Microbiological Quality ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Low Grade Inflammation ◽  
Additional Role

The role of various factors contributing to the development of systemic persistent low-grade inflammation in chronic kidney disease (CKD) is considered. It is reported that inflammation in patients with CKD is directly correlated with the glomerular filtration rate (GFR) and culminates in the terminal stage of renal failure, where extracorporeal factors such as dialysate contaminants, dialysate microbiological quality and the biocompatibility of factors in the dialysis chain play an additional role. The effectiveness of therapeutic interventions aimed at correcting inflammation in patients with CKD is discussed. Further investigations are needed to evaluate the effects of these interventions on hard outcomes, as well as to better understand the role of inflammation in selected CKD populations, particularly in children.

scholarly journals Gut microbiota alterations in patients with persistent respiratory dysfunction three months after severe COVID-19

2021 ◽  
Author(s):  
Beate Vestad ◽  
Thor Ueland ◽  
Tori Vigeland Lerum ◽  
Tuva B Dahl ◽  
Kristian Holm ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Rrna Gene ◽  
Low Grade ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Respiratory Dysfunction ◽  
Low Grade Inflammation ◽  
Gut Microbiota Composition

Objective: Although COVID-19 is primarily a respiratory infection, mounting evidence suggests that the GI tract is involved in the disease, with gut barrier dysfunction and gut microbiota alterations being related to disease severity. Whether these alterations persist and could be related to long-term respiratory dysfunction is unknown. Design: From the NOR-Solidarity trial (n=181), plasma was collected during hospital admission and after three months, and analyzed for markers of gut barrier dysfunction and inflammation. At the three-month follow-up, pulmonary function was assessed by measuring diffusing capacity of the lungs for carbon monoxide (DLCO), and rectal swabs for gut microbiota analyses were collected (n= 97) and analysed by sequencing of the 16S rRNA gene. Results: Gut microbiota diversity was reduced in COVID-19 patients with persistent respiratory dysfunction, defined as DLCO below lower limit of normal three months after hospitalization. These patients also had an altered global gut microbiota composition, with reduced abundance of Erysipelotrichaceae UCG-003 and increased abundance of Flavonifractor and Veillonella, the latter potentially being linked to fibrosis. During hospitalization, increased plasma levels of lipopolysaccharide-binding protein (LBP) were strongly associated with respiratory failure, defined as pO2/fiO2-(P/F-ratio)<26.6 kPa. LBP levels remained elevated during and after hospitalization, and was associated with low-grade inflammation and persistent respiratory dysfunction after three months. Conclusion: Persistent respiratory dysfunction after COVID-19 is associated with reduced biodiversity and gut microbiota alterations, along with persistently elevated LBP levels. Our results point to a potential gut-lung axis that should be further investigated in relation to long-term pulmonary dysfunction and long COVID.

scholarly journals Metabolite Signature of Albuminuria Involves Amino Acid Pathways in 8661 Finnish Men Without Diabetes

2020 ◽  
Vol 106 (1) ◽  
pp. 143-152
Author(s):  
Lilian Fernandes Silva ◽  
Jagadish Vangipurapu ◽  
Ulf Smith ◽  
Markku Laakso
Keyword(s):  
Chronic Kidney Disease ◽  
Insulin Secretion ◽  
Amino Acid ◽  
Insulin Sensitivity ◽  
Kidney Disease ◽  
Amino Acid Metabolism ◽  
Acid Metabolism ◽  
Low Grade ◽  
Follow Up Study

Abstract Objective To investigate the metabolite signature of albuminuria in individuals without diabetes or chronic kidney disease to identify possible mechanisms that result in increased albuminuria and elevated risk of type 2 diabetes (T2D). Research Design and Methods The study cohort was a population-based Metabolic Syndrome In Men (METSIM) study including 8861 middle-aged and elderly Finnish men without diabetes or chronic kidney disease at baseline. A total of 5504 men participated in a 7.5-year follow-up study, and 5181 of them had metabolomics data measured by Metabolon’s ultrahigh performance liquid chromatography-tandem mass spectroscopy. Results We found 32 metabolites significantly (P &lt; 5.8 × 10-5) and positively associated with the urinary albumin excretion (UAE) rate. These metabolites were especially downstream metabolites in the amino acid metabolism pathways (threonine, phenylalanine, leucine, arginine). In our 7.5-year follow-up study, UAE was significantly associated with a 19% increase (hazard ratio 1.19; 95% confidence interval, 1.13–1.25) in the risk of T2D after the adjustment for confounding factors. Conversion to diabetes was more strongly associated with a decrease in insulin secretion than a decrease in insulin sensitivity. Conclusions Metabolic signature of UAE included multiple metabolites, especially from the amino acid metabolism pathways known to be associated with low-grade inflammation, and accumulation of reactive oxygen species that play an important role in the pathogenesis of UAE. These metabolites were primarily associated with an increase in UAE and were secondarily associated with a decrease in insulin secretion and insulin sensitivity, resulting in an increased risk of incident T2D.

scholarly journals Dietary sulfate-driven and gut dysbiosis-triggered breast cancer-related gene upregulation

2018 ◽  
Author(s):  
CHEN YanPingf ◽  
LIAO Tao ◽  
TAN LiLi ◽  
CHEN DongMei ◽  
XU Qin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gut Microbiota ◽  
Individual Difference ◽  
Suppressor Gene ◽  
Low Grade ◽  
Ki 67 ◽  
Cancer Related Gene ◽  
The Individual ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

AbstractBy gut microbiota metagenomic analysis, we found that the abundance of sulfatase-secreting bacteria (SSB) in the gut of mice fed chondroitin sulfate (CS) increases with significant individual difference. The fluctuation of lipopolysaccharide (LPS) and pro-inflammatory indicators with significant individual and tissue variations was also observed. After mice were fed mixed with CS or injected separately with LPS, the breast cancer-related transcriptional factor genes, BCL11A and RUNX1, were upregulated, whereas the tumor suppressor gene, TP53BP1, were downregulated. Further, the mammary myopithelium marker CK5/6, the mammary hyperplasia marker Ki-67, and other tumor markers were also upregulated. While the exogenous estradiol does not induce the expression of BCL11A, RUNX1, and TP53BP1, the estrogen receptor (ER) agonist Fulvestrant that mimics estradiol action not only elevates estradiol concentrations, but also upregulates tumor marker expression levels, revealing that ER inflammatory inactivation and hyperestrogenemia induction might be the etiological cues of breast cancer origin. This study has preliminarily established a possible correlation of gut microbiota dysbiosis and chronic low-grade inflammation with the early-phase onset of breast cancer in mice. The statistical insignificance of test data was attributed to the individual difference of gut microbiota compositions, which determining the individual and tissue variations of systemic inflammation.

scholarly journals Arterial Remodelling in Chronic Kidney Disease: Impact of Uraemic Toxins and New Pharmacological Approaches

2021 ◽  
Vol 10 (17) ◽  
pp. 3803
Author(s):  
Nabil Foudi ◽  
Maeva Palayer ◽  
Marie Briet ◽  
Anne-Sophie Garnier
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Health Concern ◽  
Low Grade ◽  
Large Artery ◽  
Vascular Health ◽  
Cell Functions ◽  
High Prevalence ◽  
Disease Impact ◽  
Low Grade Inflammation

Chronic kidney disease (CKD) is a major public health concern that affects around 10 percent of the world’s population. The severity of CKD is mainly due to the high prevalence of cardiovascular (CV) complications in this population. The aim of this review is to describe the arterial remodelling associated with CKD, to provide a quick overview of the mechanisms involved and to review the recent pharmacological approaches aimed at improving vascular health in CKD. CKD patients are exposed to metabolic and haemodynamic disorders that may affect the CV system. Large artery functional and geometric abnormalities have been well documented in CKD patients and are associated with an increase in arterial stiffness and a maladaptive remodelling. Uraemic toxins, such as indoxyl sulphate, p-cresyl sulphate, protein carbamylation and advanced glycation products, exert various effects on vascular smooth muscle cell functions. The low-grade inflammation associated with CKD may also affect arterial wall composition and remodelling. It is worth noting that the CV risk for CKD patients remains high despite the pharmacological control of traditional CV risk factors, suggesting the need for innovative therapeutic strategies. An interventional study targeting the NLRP3 inflammasome has provided some interesting preliminary results that need to be confirmed, especially in terms of safety.

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