Inflammatory bowel diseases (IBDs) are chronic diseases of gastrointestinal tract, characterized by inflammation and mucosal damage. As IBD is known to associate with complex crosstalk between immune response and oxidative stress, and thus the extraintestinal manifestations crossed to other organs are commonly investigated1. Dextran sulfate sodium (DSS)-induced colitis closely approximating to human IBD is a widely used model of intestinal inflammation. Recently DSS-colitis is reported to induce kidney inflammation through IL-62. However, neither renal injury nor renal extracellular matrix (ECM) change after DSS-colitis induction is still unknown. The aim of this study is to investigate the influence of DSS-induced colitis on renal injury and ECM change, and to elucidate the relationship between inflammation and ECM remodeling. ICR male mice (28-30g, n=6) were used as acute colitis animal model by treating with 3.5% (w/v) DSS in drinking water, and those with water were used as control. After 8 day DSS treatment, mice were anesthetized with pentobarbital (60 mg/kg, i.v) and body weight measurement, detection of renal function, histological damages and renal ECM deposition were further conducted. All detected values are represented as means ± S.E.M., compared by unpaired t test. The results showed that 15% of body weight lost as compared to control (p <0.05), and serum BUN level raised up to 40.92 ± 4.08 whereas only 18.57 ± 0.44 for control (p <0.05). H&E staining showed swelling renal tubules and high-level neutrophil/monocyte infiltration in both colon and renal tissues, proving both colitis and renal inflammations were induced by DSS. Western blotting analysis on renal cortex indicated the values of inflammation cytokines of IL-6, TNF-α, and inflammation mediators of COX-2, iNOS were 2.64 ± 0.39, 1.63 ± 0.143, 1.35 ± 0.06, and 1.82 ± 0.24, respectively, as compared to those of control (p<0.05). Moreover, values of protein expression of nephrin and podocalyxin in podocyte, and VE-cadherin in glomerular capillary were 0.52 ± 0.05, 0.48 ± 0.11, and 0.81 ± 0.04, respectively (p<0.05), indicating that renal inflammation may led to dysfunction on podocyte and glomerular capillary. PAS and Masson’s staining showed renal glomerular mesangial matrix expansion, vascular adventitia as well as thickening on glomerular basement membrane and proximal tubules. In addition, ECMs in cortex such as collagens I and V showed increasing values of 1.35 ± 0.05 and 1.37 ± 0.06, respectively (p<0.05), whereas collagen IV and fibronectin showed decreasing values of 0.46 ± 0.016 and 0.44 ± 0.07, respectively (p<0.05). These facts imply that DSS-induced colitis contributes to renal inflammatory injury, leads to podocyte dysfunction, renal basement membrane damage, and affect renal ECM remodeling.