FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2766277535> ?p ?o ?g. }

• W2766277535 endingPage "27" @default.
• W2766277535 startingPage "13" @default.
• W2766277535 abstract "ObjectiveCardiovascular disease is the leading cause of death in kidney transplant recipients (KTRs), yet incompletely accountable by traditional risk factors. Inflammation is an unconventional cardiovascular risk factor, with gut-derived endotoxemia potentially driving inflammation and endothelial disease. Comparable data are lacking in kidney transplantation. This study investigated the associations of endotoxemia with inflammation, endothelial activation, and 5-year cardiovascular events in KTRs. Determinants of endotoxemia were also explored.Design and MethodsThis is a single-center cross-sectional study with prospective follow-up from a prevalent cohort of 128 KTRs.Main Outcome MeasuresDemographic, nutritional and clinical predictors of inflammation (high-sensitivity C-reactive protein [hsCRP]), endothelial activation (sE-selectin), and endotoxemia (endotoxin) were assessed. Follow-up data on 5-year cardiovascular event rates were collected.ResultsEndotoxemia (P = .03), reduced 25-hydroxyvitamin D (P = .04), high fructose intake (P < .001), decreased fiber intake (P < .001), and abdominal obesity (P = .002) were independently associated with elevated hsCRP. In turn, endotoxemia (P = .007) and increasing hsCRP (P = .02) were both independently associated with raised sE-selectin. Furthermore, endotoxemia predicted increased cardiovascular event rate (P = .02), independent of hsCRP and a global measure of cardiovascular risk estimated by a validated algorithm of 7-year risk for major adverse cardiac events in kidney transplantation. Determinants of endotoxemia included reduced 25-hydroxyvitamin D (P < .001), hypertriglyceridemia (P < .001), increased fructose intake (P = .01), and abdominal obesity (P = .01).ConclusionsEndotoxemia in KTRs contributes to inflammation, endothelial activation, and increased cardiovascular events. This study highlights the clinical relevance of endotoxemia in KTRs, suggesting future interventional targets. Cardiovascular disease is the leading cause of death in kidney transplant recipients (KTRs), yet incompletely accountable by traditional risk factors. Inflammation is an unconventional cardiovascular risk factor, with gut-derived endotoxemia potentially driving inflammation and endothelial disease. Comparable data are lacking in kidney transplantation. This study investigated the associations of endotoxemia with inflammation, endothelial activation, and 5-year cardiovascular events in KTRs. Determinants of endotoxemia were also explored. This is a single-center cross-sectional study with prospective follow-up from a prevalent cohort of 128 KTRs. Demographic, nutritional and clinical predictors of inflammation (high-sensitivity C-reactive protein [hsCRP]), endothelial activation (sE-selectin), and endotoxemia (endotoxin) were assessed. Follow-up data on 5-year cardiovascular event rates were collected. Endotoxemia (P = .03), reduced 25-hydroxyvitamin D (P = .04), high fructose intake (P < .001), decreased fiber intake (P < .001), and abdominal obesity (P = .002) were independently associated with elevated hsCRP. In turn, endotoxemia (P = .007) and increasing hsCRP (P = .02) were both independently associated with raised sE-selectin. Furthermore, endotoxemia predicted increased cardiovascular event rate (P = .02), independent of hsCRP and a global measure of cardiovascular risk estimated by a validated algorithm of 7-year risk for major adverse cardiac events in kidney transplantation. Determinants of endotoxemia included reduced 25-hydroxyvitamin D (P < .001), hypertriglyceridemia (P < .001), increased fructose intake (P = .01), and abdominal obesity (P = .01). Endotoxemia in KTRs contributes to inflammation, endothelial activation, and increased cardiovascular events. This study highlights the clinical relevance of endotoxemia in KTRs, suggesting future interventional targets." @default.
• W2766277535 created "2017-11-10" @default.
• W2766277535 creator A5000172660 @default.
• W2766277535 creator A5012147929 @default.
• W2766277535 creator A5025922625 @default.
• W2766277535 creator A5027846091 @default.
• W2766277535 creator A5028462984 @default.
• W2766277535 creator A5039450642 @default.
• W2766277535 creator A5047920650 @default.
• W2766277535 creator A5057591951 @default.
• W2766277535 creator A5065000534 @default.
• W2766277535 creator A5087023083 @default.
• W2766277535 date "2018-01-01" @default.
• W2766277535 modified "2023-10-15" @default.
• W2766277535 title "The Associations of Endotoxemia With Systemic Inflammation, Endothelial Activation, and Cardiovascular Outcome in Kidney Transplantation" @default.
• W2766277535 cites W1490290899 @default.
• W2766277535 cites W1523685166 @default.
• W2766277535 cites W1535151445 @default.
• W2766277535 cites W1572463134 @default.
• W2766277535 cites W1580333814 @default.
• W2766277535 cites W1849785625 @default.
• W2766277535 cites W1966381719 @default.
• W2766277535 cites W1972919038 @default.
• W2766277535 cites W1973538008 @default.
• W2766277535 cites W1978984225 @default.
• W2766277535 cites W1981559442 @default.
• W2766277535 cites W1982547579 @default.
• W2766277535 cites W1987944767 @default.
• W2766277535 cites W1991539495 @default.
• W2766277535 cites W1992471429 @default.
• W2766277535 cites W1999946358 @default.
• W2766277535 cites W2000136255 @default.
• W2766277535 cites W2003942863 @default.
• W2766277535 cites W2004841610 @default.
• W2766277535 cites W2005970630 @default.
• W2766277535 cites W2007048225 @default.
• W2766277535 cites W2010413021 @default.
• W2766277535 cites W2011747906 @default.
• W2766277535 cites W2013480262 @default.
• W2766277535 cites W2017948978 @default.
• W2766277535 cites W2020279050 @default.
• W2766277535 cites W2027340093 @default.
• W2766277535 cites W2029643995 @default.
• W2766277535 cites W2030407395 @default.
• W2766277535 cites W2035885128 @default.
• W2766277535 cites W2036122623 @default.
• W2766277535 cites W2038795938 @default.
• W2766277535 cites W2046345722 @default.
• W2766277535 cites W2046879590 @default.
• W2766277535 cites W2049036131 @default.
• W2766277535 cites W2049288350 @default.
• W2766277535 cites W2055572629 @default.
• W2766277535 cites W2057607705 @default.
• W2766277535 cites W2060184663 @default.
• W2766277535 cites W2065367419 @default.
• W2766277535 cites W2066565213 @default.
• W2766277535 cites W2075536991 @default.
• W2766277535 cites W2078395019 @default.
• W2766277535 cites W2091805179 @default.
• W2766277535 cites W2093486057 @default.
• W2766277535 cites W2099246760 @default.
• W2766277535 cites W2102259217 @default.
• W2766277535 cites W2106384954 @default.
• W2766277535 cites W2109302289 @default.
• W2766277535 cites W2115432010 @default.
• W2766277535 cites W2119407544 @default.
• W2766277535 cites W2121315929 @default.
• W2766277535 cites W2124120768 @default.
• W2766277535 cites W2124900012 @default.
• W2766277535 cites W2126101166 @default.
• W2766277535 cites W2128899692 @default.
• W2766277535 cites W2128976540 @default.
• W2766277535 cites W2129917444 @default.
• W2766277535 cites W2133010654 @default.
• W2766277535 cites W2133808995 @default.
• W2766277535 cites W2134141918 @default.
• W2766277535 cites W2138132326 @default.
• W2766277535 cites W2140694676 @default.
• W2766277535 cites W2140697034 @default.
• W2766277535 cites W2147397909 @default.
• W2766277535 cites W2147730333 @default.
• W2766277535 cites W2147931984 @default.
• W2766277535 cites W2153406190 @default.
• W2766277535 cites W2156796015 @default.
• W2766277535 cites W2157243060 @default.
• W2766277535 cites W2161096570 @default.
• W2766277535 cites W2161424641 @default.
• W2766277535 cites W2162696374 @default.
• W2766277535 cites W2168244623 @default.
• W2766277535 cites W2171536994 @default.
• W2766277535 cites W2253134880 @default.
• W2766277535 cites W82042788 @default.
• W2766277535 doi "https://doi.org/10.1053/j.jrn.2017.06.004" @default.
• W2766277535 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29089280" @default.
• W2766277535 hasPublicationYear "2018" @default.
• W2766277535 type Work @default.
• W2766277535 sameAs 2766277535 @default.
• W2766277535 citedByCount "5" @default.

• next