{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:09:08Z","timestamp":1790222948299,"version":"4.1.0"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,7,15]]},"abstract":"<jats:p> Adenine overload promotes intratubular crystal precipitation and interstitial nephritis. We showed recently that these abnormalities are strongly attenuated in mice knockout for Toll-like receptors-2, -4, MyD88, ASC, or caspase-1. We now investigated whether NF-\u03baB activation also plays a pathogenic role in this model. Adult male Munich-Wistar rats were distributed among three groups: C ( n = 17), receiving standard chow; ADE ( n = 17), given adenine in the chow at 0.7% for 1 wk and 0.5% for 2 wk; and ADE + pyrrolidine dithiocarbamate (PDTC; n = 14), receiving adenine as above and the NF-\u03baB inhibitor PDTC (120 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> in the drinking water). After 3 wk, widespread crystal deposition was seen in tubular lumina and in the renal interstitium, along with granuloma formation, collagen accumulation, intense tubulointerstitial proliferation, and increased interstitial expression of inflammatory mediators. Part of the crystals were segregated from tubular lumina by a newly formed cell layer and, at more advanced stages, appeared to be extruded to the interstitium. p65 nuclear translocation and IKK-\u03b1 increased abundance indicated activation of the NF-\u03baB system. PDTC treatment prevented p65 migration and normalized IKK-\u03b1, limited crystal shift to the interstitium, and strongly attenuated interstitial fibrosis\/inflammation. These findings indicate that the complex inflammatory phenomena associated with this model depend, at least in part, on NF-\u03baB activation, and suggest that the NF-\u03baB system may become a therapeutic target in the treatment of chronic kidney disease. <\/jats:p>","DOI":"10.1152\/ajprenal.00491.2012","type":"journal-article","created":{"date-parts":[[2013,5,9]],"date-time":"2013-05-09T03:59:31Z","timestamp":1368071971000},"page":"F155-F163","source":"Crossref","is-referenced-by-count":36,"title":["NF-\u03baB activation mediates crystal translocation and interstitial inflammation in adenine overload nephropathy"],"prefix":"10.1152","volume":"305","author":[{"given":"Cristiene","family":"Okabe","sequence":"first","affiliation":[{"name":"Renal Division, Department of Clinical Medicine, Faculty of Medicine, University of S\u00e3o Paulo S\u00e3o Paulo, Brazil; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raquel Lerner","family":"Borges","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Clinical Medicine, Faculty of Medicine, University of S\u00e3o Paulo S\u00e3o Paulo, Brazil; 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