FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4229041029> ?p ?o ?g. }

• W4229041029 abstract "Abstract BACKGROUND AND AIMS Chronic inflammation is common in patients with chronic kidney disease (CKD) and is associated with poor outcomes. Although the etiology is only partly understood, the gut–kidney axis is considered an important contributor [1]. Lipopolysaccharide (LPS), also known as endotoxin, is a well-characterized pyrogen found in the exterior cell membrane of most of the gram-negative bacteria. It plays an important role in promoting intestinal inflammatory responses. When absorbed through the intestinal epithelium, LPS induces inflammation by activating macrophages and monocytes. Due to short half-life and semi-quantitative assay characteristics of the Limulus Amebocyte Lysate (LAL) assay, direct quantification of LPS is not suitable to quantify activation of the innate immune system. Lipoprotein-binding protein (LBP), a more stable biomarker, is an acute phase protein produced mostly by the hepatocytes and intestinal epithelial cells and is an essential component of an effective innate immune response to LPS. Circulating LBP significantly enhances the sensitivity of CD14 + cells (mostly monocytes and macrophages) to stimulation by LPS. LBP has been shown to facilitate binding of LPS to CD14 receptor. Levels of LBP peak in serum shortly after endotoxemia and remain increased up to 72 h later. An increased plasma LBP indicates gut epithelial barrier dysfunction [2]. Whether LBP is altered by CKD is not known. METHOD We analyzed the effects of CKD on LBP plasma concentrations. We used samples from the Leuven mild-to-moderate CKD cohort (NCT00441623). To study causality, we used animal models of experimentally induced CKD. To exclude model-related bias, two different rat models of CKD, i.e. 5/6th nephrectomy and adenine supplementation, were used. LBP was measured using commercially available ELISA kits (Hycultbiotech, The Netherlands). RESULTS In a cohort of 460 patients with CKD, we found a significant increase in LBP levels across the different stages of CKD (ANOVA, P: 0.001). When analyzed as a continuous variable, LBP is significantly inversely correlated with eGFR (P &lt; 0.001; Spearman, r: −0.221), and positively correlated with CRP (P &lt; 0.001; Spearman, r: 0.592). During a median follow-up of 56 (IQR, 53–59) months, 70 patients died, with more deaths observed among patients with LBP in higher tertiles [tertiles 1–3: 11, 22, and 37 events, respectively (Fig. 1)]. In univariate Cox proportional hazard analysis, plasma LBP was significantly associated with mortality [hazard ratio (HR) of 1.032; 95% confidence interval (95% CI): 1.014– 1.046; P &lt; 0.001). This association remained significant in multivariate models with adjustment for age, sex and BMI. In two different rat models, induction of CKD resulted in a significant increase in LBP (P &lt; 0.001). In these animals, we observed a significant inverse association between eGFR (and measured creatinine clearance) and LBP concentrations (P &lt; 0.001; Spearman, r: −0.460). CONCLUSION Patients with CKD have higher levels of LBP, with higher levels of plasma LBP present in patients with more advanced CKD. Plasma LBP is an independent predictor of mortality. Experimentally induced CKD equally results in significantly increased LBP. Our data suggest that CKD leads to increased passage of LPS across the intestinal barrier. These findings strengthen the hypothesis of the gut–kidney axis as a source of chronic inflammation." @default.
• W4229041029 created "2022-05-08" @default.
• W4229041029 creator A5009144215 @default.
• W4229041029 creator A5014294387 @default.
• W4229041029 creator A5022450532 @default.
• W4229041029 creator A5057862603 @default.
• W4229041029 creator A5083782401 @default.
• W4229041029 date "2022-05-01" @default.
• W4229041029 modified "2023-10-06" @default.
• W4229041029 title "MO587: Chronic Kidney Disease Induces Endotoxin-Related Activation of The Innate Immune System" @default.
• W4229041029 doi "https://doi.org/10.1093/ndt/gfac074.032" @default.
• W4229041029 hasPublicationYear "2022" @default.
• W4229041029 type Work @default.
• W4229041029 citedByCount "0" @default.
• W4229041029 crossrefType "journal-article" @default.
• W4229041029 hasAuthorship W4229041029A5009144215 @default.
• W4229041029 hasAuthorship W4229041029A5014294387 @default.
• W4229041029 hasAuthorship W4229041029A5022450532 @default.
• W4229041029 hasAuthorship W4229041029A5057862603 @default.
• W4229041029 hasAuthorship W4229041029A5083782401 @default.
• W4229041029 hasBestOaLocation W42290410291 @default.
• W4229041029 hasConcept C126322002 @default.
• W4229041029 hasConcept C136449434 @default.
• W4229041029 hasConcept C203014093 @default.
• W4229041029 hasConcept C2776040547 @default.
• W4229041029 hasConcept C2776822972 @default.
• W4229041029 hasConcept C2776914184 @default.
• W4229041029 hasConcept C2778384902 @default.
• W4229041029 hasConcept C2778513237 @default.
• W4229041029 hasConcept C2778653478 @default.
• W4229041029 hasConcept C2778754761 @default.
• W4229041029 hasConcept C2781197716 @default.
• W4229041029 hasConcept C55493867 @default.
• W4229041029 hasConcept C57194454 @default.
• W4229041029 hasConcept C71924100 @default.
• W4229041029 hasConcept C86803240 @default.
• W4229041029 hasConcept C8891405 @default.
• W4229041029 hasConceptScore W4229041029C126322002 @default.
• W4229041029 hasConceptScore W4229041029C136449434 @default.
• W4229041029 hasConceptScore W4229041029C203014093 @default.
• W4229041029 hasConceptScore W4229041029C2776040547 @default.
• W4229041029 hasConceptScore W4229041029C2776822972 @default.
• W4229041029 hasConceptScore W4229041029C2776914184 @default.
• W4229041029 hasConceptScore W4229041029C2778384902 @default.
• W4229041029 hasConceptScore W4229041029C2778513237 @default.
• W4229041029 hasConceptScore W4229041029C2778653478 @default.
• W4229041029 hasConceptScore W4229041029C2778754761 @default.
• W4229041029 hasConceptScore W4229041029C2781197716 @default.
• W4229041029 hasConceptScore W4229041029C55493867 @default.
• W4229041029 hasConceptScore W4229041029C57194454 @default.
• W4229041029 hasConceptScore W4229041029C71924100 @default.
• W4229041029 hasConceptScore W4229041029C86803240 @default.
• W4229041029 hasConceptScore W4229041029C8891405 @default.
• W4229041029 hasIssue "Supplement_3" @default.
• W4229041029 hasLocation W42290410291 @default.
• W4229041029 hasOpenAccess W4229041029 @default.
• W4229041029 hasPrimaryLocation W42290410291 @default.
• W4229041029 hasRelatedWork W1557621914 @default.
• W4229041029 hasRelatedWork W1648631879 @default.
• W4229041029 hasRelatedWork W1932660839 @default.
• W4229041029 hasRelatedWork W1979595130 @default.
• W4229041029 hasRelatedWork W2040642611 @default.
• W4229041029 hasRelatedWork W2041692577 @default.
• W4229041029 hasRelatedWork W2045769288 @default.
• W4229041029 hasRelatedWork W2133218406 @default.
• W4229041029 hasRelatedWork W2166108529 @default.
• W4229041029 hasRelatedWork W4229041029 @default.
• W4229041029 hasVolume "37" @default.
• W4229041029 isParatext "false" @default.
• W4229041029 isRetracted "false" @default.
• W4229041029 workType "article" @default.