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We studied how acute intestinal injury affects the kidneys and the kallikrein\u2010kinin system in mice with dextran sodium sulfate (DSS)\u2010induced colitis. Seven\u2010week\u2010old male BALB\/c mice were treated with 5% DSS for 7\u2009days and either sacrificed immediately (DSS7, <jats:italic>n<\/jats:italic>\u2009=\u20096) or given fresh water for 4 more days (DSS11, <jats:italic>n<\/jats:italic>\u2009=\u20096). Untreated mice (n\u2009=\u20096) served as controls. Colitis and kidney damage was assessed using histochemical and immunohistochemical staining, ELISA, and RT\u2010qPCR. Markers of kidney injury correlated with markers of colitis. Colitis increased albuminuria, reduced kidney weight, and induced transcription of <jats:italic>lipocalin 2<\/jats:italic>, <jats:italic>kidney injury molecule\u20101<\/jats:italic>, and <jats:italic>interleukin\u20101beta<\/jats:italic>, as well as increased immunostaining signal of c\u2010Jun and NF\u2010\u03baB p65 in the kidneys. Colitis caused strong induction of colonic <jats:italic>kininogen 2<\/jats:italic> transcription and bradykinin receptor B1\u2010positive cells in the disrupted mucosa. In the kidney, colitis induced localization of tubular bradykinin receptor B2 to the nuclear envelope and increased <jats:italic>kininogen 2<\/jats:italic> transcription. Disruption of the intestinal barrier by DSS promotes markers of kidney injury and inflammation, and the degree of kidney injury correlates with the severity of colitis. Colitis is associated with increased expression of kallikrein\u2010kinin components in both the colon and kidneys.<\/jats:p>","DOI":"10.14814\/phy2.70161","type":"journal-article","created":{"date-parts":[[2025,3,4]],"date-time":"2025-03-04T11:45:00Z","timestamp":1741088700000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Dextran sodium sulfate\u2010induced colitis in male <scp>BALB<\/scp>\/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney"],"prefix":"10.14814","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3418-152X","authenticated-orcid":false,"given":"Hanne","family":"Salmenkari","sequence":"first","affiliation":[{"name":"Folkh\u00e4lsan Research Center  Helsinki Finland"},{"name":"Research Program for Clinical and Molecular Metabolism University of Helsinki  Helsinki Finland"},{"name":"Department of Nephrology University of Helsinki and 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