PMID- 23307618
OWN - NLM
STAT- MEDLINE
DCOM- 20140826
LR  - 20151119
IS  - 1099-1263 (Electronic)
IS  - 0260-437X (Linking)
VI  - 34
IP  - 2
DP  - 2014 Feb
TI  - Early detection of renal injury using urinary vanin-1 in rats with experimental 
      colitis.
PG  - 184-90
LID - 10.1002/jat.2849 [doi]
AB  - Renal complications are often detected in patients with inflammatory bowel 
      disease (IBD). Because conventional markers such as serum creatinine and 
      beta2-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.
CI  - Copyright (c) 2013 John Wiley & Sons, Ltd.
FAU - Hosohata, Keiko
AU  - Hosohata K
AD  - Division of Clinical Pharmacology, Department of Pharmacology, School of 
      Medicine, Jichi Medical University, Tochigi, 329-0498, Japan.
FAU - Ando, Hitoshi
AU  - Ando H
FAU - Fujimura, Akio
AU  - Fujimura A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130111
PL  - England
TA  - J Appl Toxicol
JT  - Journal of applied toxicology : JAT
JID - 8109495
RN  - 0 (Biomarkers)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (GPI-Linked Proteins)
RN  - 0 (Havcr1protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid)
RN  - AYI8EX34EU (Creatinine)
RN  - EC 3.2.1.52 (Acetylglucosaminidase)
RN  - EC 3.5.- (Amidohydrolases)
RN  - EC 3.5.1.- (pantetheinase)
SB  - IM
MH  - Acetylglucosaminidase/urine
MH  - Amidohydrolases/*urine
MH  - Animals
MH  - Biomarkers/blood/urine
MH  - Cell Adhesion Molecules/urine
MH  - Chemokine CCL2/urine
MH  - Colitis/chemically induced/pathology/*urine
MH  - Colon/drug effects/metabolism
MH  - Creatinine/blood
MH  - Disease Models, Animal
MH  - Early Diagnosis
MH  - GPI-Linked Proteins/urine
MH  - Kidney/drug effects/metabolism
MH  - Kidney Diseases/*diagnosis
MH  - Kidney Function Tests
MH  - Male
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Trinitrobenzenesulfonic Acid
OTO - NOTNLM
OT  - TNBS
OT  - experimental model
OT  - inflammatory bowel disease
OT  - renal complications
OT  - urinary biomarker
EDAT- 2013/01/12 06:00
MHDA- 2014/08/27 06:00
CRDT- 2013/01/12 06:00
PHST- 2012/08/15 00:00 [received]
PHST- 2012/11/12 00:00 [revised]
PHST- 2012/11/13 00:00 [accepted]
PHST- 2013/01/12 06:00 [entrez]
PHST- 2013/01/12 06:00 [pubmed]
PHST- 2014/08/27 06:00 [medline]
AID - 10.1002/jat.2849 [doi]
PST - ppublish
SO  - J Appl Toxicol. 2014 Feb;34(2):184-90. doi: 10.1002/jat.2849. Epub 2013 Jan 11.