{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T14:05:58Z","timestamp":1784210758202,"version":"3.55.0"},"reference-count":37,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,2,12]],"date-time":"2013-02-12T00:00:00Z","timestamp":1360627200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"MRC, UK"},{"name":"Egyptian fellowship"},{"name":"Marie Curie Fellowship"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2013,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Patients with cirrhosis frequently develop renal dysfunction, a proportion of who do not fulfill criteria for hepatorenal syndrome (<jats:styled-content style=\"fixed-case\">HRS<\/jats:styled-content>). We hypothesized that the kidneys in these patients would exhibit histological and biomarker evidence of kidney injury. We looked specifically for <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content> expression as they may mediate kidney injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Sixty seven subjects (6); alcoholic cirrhosis: compensated (9), acute deterioration of alcoholic cirrhosis (52)] were included. Renal dysfunction was defined as a creatinine of &gt;133\u00a0\u03bcmol\/L and\/or according to the <jats:styled-content style=\"fixed-case\">AKI<\/jats:styled-content> network criteria. Urinary biomarkers, <jats:styled-content style=\"fixed-case\">KIM<\/jats:styled-content>\u20101, \u03c0<jats:styled-content style=\"fixed-case\">GST<\/jats:styled-content>, \u03b1<jats:styled-content style=\"fixed-case\">GST<\/jats:styled-content> and a novel biomarker, urinary <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 were measured. Renal biopsies were also available from eight other alcoholic cirrhosis patients (three non\u2010<jats:styled-content style=\"fixed-case\">HRS<\/jats:styled-content> renal dysfunction; five <jats:styled-content style=\"fixed-case\">HRS<\/jats:styled-content>) that were stained for <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 and caspase\u20103.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Fourteen patients developed renal dysfunction, amongst these three had type 2 <jats:styled-content style=\"fixed-case\">HRS<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">KIM<\/jats:styled-content>\u20101, \u03c0<jats:styled-content style=\"fixed-case\">GST<\/jats:styled-content> and \u03b1<jats:styled-content style=\"fixed-case\">GST<\/jats:styled-content> were higher in patients with acute deterioration of cirrhosis compared with patients with compensated cirrhosis, but did not differ between those with and without renal dysfunction. Urinary <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 was significantly higher in patients with renal dysfunction associated with infection\/inflammation. Kidney biopsies from non\u2010<jats:styled-content style=\"fixed-case\">HRS<\/jats:styled-content> renal dysfunction patients showed tubular damage with evidence of increased tubular expression of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4, and caspase\u20103. Minor changes were observed in <jats:styled-content style=\"fixed-case\">HRS<\/jats:styled-content> patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The data provide proof of concept that renal dysfunction in patients with cirrhosis with superimposed inflammation is associated with significant tubular injury and apoptosis and with increased renal expression and urinary excretion of the <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4, suggesting a potential role of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 as mediator of renal injury.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12047","type":"journal-article","created":{"date-parts":[[2012,11,12]],"date-time":"2012-11-12T10:40:04Z","timestamp":1352716804000},"page":"398-409","source":"Crossref","is-referenced-by-count":113,"title":["Increased renal expression and urinary excretion of <scp>TLR<\/scp>4 in acute kidney injury associated with 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