Early detection of renal injury using urinary vanin-1 in rats with experimental colitis.

Renal complications are often detected in patients with inflammatory bowel disease (IBD). Because conventional markers such as serum creatinine and β2-microglobulin are not sensitive and/or specific, a new renal biomarker is needed. We have recently identified urinary vanin-1 as an early biomarker for the detection of nephrotoxicant-induced renal injury. In this study, we compared the usefulness of urinary vanin-1 with other newly developed biomarkers [urinary monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (Kim-1) and N-acetyl-beta-D-glucosaminidase (NAG)] for the detection of renal complications in rats with experimental colitis. On day 2 after intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), male Wistar rats developed not only colitis, but histologically evident renal injury. Urinary vanin-1 started to elevate on day 1, whereas serum creatinine and urinary excretions of glucose, total protein, albumin, Kim-1, MCP-1 and NAG significantly increased only on day 2. The mRNA expressions of vanin-1 and Kim-1 significantly increased in the kidney, but not in the colon. In addition, vanin-1 did not appear in the blood. On the other hand, colonic mRNA expression and the serum concentration of MCP-1 were significantly higher in the TNBS-treated rats than in the control animals. These results suggest that, in contrast to MCP-1, urinary vanin-1 and Kim-1 mainly originated from the kidney rather than the colon in this model. Compared with Kim-1 and MCP-1, vanin-1 might be an earlier biomarker for the detection of renal injury in rats with experimental colitis.