We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Ketamine induced renal fibrosis in a ketamine addition rat model.
- Authors
Jang, Mei-Yu; Shen, Jung-Tsung; Geng, Jiun-Hung; Wang, Hsun-Shuan; Chuang, Shu-Mien; Lee, Yung-Chin; Lee, Chien-Te; Lee, Yi-Lun; Wu, Wen-Jeng; Juan, Yung-Shun
- Abstract
Objective The toxicity of ketamine to the genitourinary system not only involves the lower urinary tract but also the upper urinary tracts. Reports showed that ketamine abuse may cause hydronephrosis and renal function deterioration. However, the exact pathophysiological mechanism of renal injury has not been investigated. The aim of the present study is to investigate the renal injury after ketamine addition in an animal model. Materials and methods Thirty Sprague–Dawley rats were divided into three groups: control group, K-14D group, and K-28D group. The K-14D and K-28D groups received ketamine (25 mg/kg/d, intraperitoneally) through daily injections for a period of 14 days and 28 days, respectively. Masson's trichrome stains were carried out to show the histological changes. Western blotting and reverse transcription polymerase chain reaction were carried out to examine the expressions of profibrosis markers and fibrosis-associated proteins. Results Masson's trichrome stain showed that no significant renal hydronephrosis occurred after ketamine treatment. However, ketamine treatment increased the fibrosis of the tubule-interstitium and increased collagen deposition and fibronectin expression. These alterations were accompanied by increases in the expression of inflammatory and fibrosis markers, fibronectin, and type I collagen after ketamine treatment. The profibrosis marker, transforming growth factor-β (TGF-β), increased significantly after 14 days and 28 days of ketamine treatment both in terms of mRNA and protein levels. Conclusion Ketamine treatment not only induced cystitis-like syndrome, but also renal fibrosis. These renal interstitial fibrosis changes may be induced by the TGF-β pathway. These preliminary results can provide valuable information from a clinical perspective.
- Publication
Urological Science, 2017, Vol 28, Issue 3, p123
- ISSN
1879-5226
- Publication type
Article
- DOI
10.1016/j.urols.2016.12.004