Dextran sodium sulfate‐induced colitis in male <scp>BALB</scp>/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney

Inflammatory molecules originating from an inflamed gut can promote systemic inflammation. We studied how acute intestinal injury affects the kidneys and the kallikrein-kinin system in mice with dextran sodium sulfate (DSS)-induced colitis. Seven-week-old male BALB/c mice were treated with 5% DSS for 7 days and either sacrificed immediately (DSS7, n = 6) or given fresh water for 4 more days (DSS11, n = 6). Untreated mice (n = 6) served as controls. Colitis and kidney damage was assessed using histochemical and immunohistochemical staining, ELISA, and RT-qPCR. Markers of kidney injury correlated with markers of colitis. Colitis increased albuminuria, reduced kidney weight, and induced transcription of lipocalin 2, kidney injury molecule-1, and interleukin-1beta, as well as increased immunostaining signal of c-Jun and NF-κB p65 in the kidneys. Colitis caused strong induction of colonic kininogen 2 transcription and bradykinin receptor B1-positive cells in the disrupted mucosa. In the kidney, colitis induced localization of tubular bradykinin receptor B2 to the nuclear envelope and increased kininogen 2 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-kinin components in both the colon and kidneys.