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In a prevention study, treatment with 4-PBA from 20 weeks of age (prior to the development of renal injury) delayed the onset of albuminuria and significantly reduced additional indices of renal injury compared with vehicle-treated NZBWF1 mice at 36 weeks of age, including collagen deposition, tubular casts, renal cell apoptosis, and blood urea nitrogen (BUN) concentration. To test whether ER stress contributes to the progression of renal injury once albuminuria has developed, mice were monitored for the onset of albuminuria (3+ or \u2265300 mg\/dl by dipstick measurement of 24-h urine sample) and once established, were either killed (onset group), or underwent 4-PBA or vehicle treatment for 4 weeks. Treatment with 4-PBA blocked the worsening of glomerular injury, reduced the number of dilated or cast-filled tubules, and reduced the number of apoptotic cells compared with vehicle-treated mice. BUN and left ventricle to bodyweight ratio (LV:BW) were also reduced by 4-PBA treatment. Renal expression of the endogenous chaperones, protein disulphide isomerase (PDI), and 78 kDa glucose-regulated protein (GRP78, also known as binding Ig protein (BiP)), were increased in 4-PBA-treated mice. Together, these results suggest a therapeutic potential for agents like 4-PBA in combating renal injury in SLE.<\/jats:p>","DOI":"10.1042\/cs20180562","type":"journal-article","created":{"date-parts":[[2019,1,7]],"date-time":"2019-01-07T19:49:37Z","timestamp":1546890577000},"page":"167-180","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Sodium 4-phenylbutyrate treatment protects against renal injury in NZBWF1 mice"],"prefix":"10.1042","volume":"133","author":[{"given":"Mathilde\u00a0L.","family":"Bonnemaison","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eileen\u00a0S.","family":"Marks-Nelson","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5672-9197","authenticated-orcid":false,"given":"Erika\u00a0I.","family":"Boesen","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2019,1,18]]},"reference":[{"key":"2021113011022760000_B1","doi-asserted-by":"publisher","first-page":"825","DOI":"10.2215\/CJN.05780616","article-title":"Update on lupus nephritis","volume":"12","author":"Almaani","year":"2017","journal-title":"Clin. 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