Time-Dependent Alterations of Vancomycin-Induced Nephrotoxicity in Mice

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  • Takigawa Masaki
    Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology Department of Pharmacy, Tokyo Metropolitan Geriatric Hospital
  • Masutomi Hirofumi
    Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology
  • Kishimoto Yuki
    Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology
  • Shimazaki Yoshitomo
    Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology Department of Pharmacy, Tokyo Metropolitan Geriatric Hospital
  • Hamano Yoshitomo
    Department of Nephrology, Tokyo Metropolitan Geriatric Hospital
  • Kondo Yoshitaka
    Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology
  • Arai Tomio
    Department of Pathology, Tokyo Metropolitan Geriatric Hospital
  • Lee Jaewon
    Department of Pharmacy, Pusan National University
  • Ishii Toshihiro
    Department of Practical Pharmacy, Faculty of Pharmaceutical Sciences, Toho University
  • Mori Yoshiko
    Department of Pharmacy, Tokyo Metropolitan Geriatric Hospital
  • Ishigami Akihito
    Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology

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<p>Vancomycin hydrochloride (VCM) is a glycopeptide antibiotic that is commonly used against methicillin-resistant, Gram-positive cocci despite the nephrotoxic side effects. VCM-induced nephrotoxicity has been reported in 5–28% of recipient patients. Therefore, renal failure induced by VCM has become an important clinical problem. However, the exceedingly complex mechanism of VCM-induced nephrotoxicity is not fully understood. Therefore, this study was designed to clarify time-dependent alterations of VCM-induced nephrotoxicity in mice as a step toward decreasing the risks of kidney injury associated with VCM therapy. VCM was injected intraperitoneally into mice at a dose of 400 mg/kg body weight at 24-h intervals for 3, 5, 7, and 14 d. At 24 h after the last injection, we examined histopathological alterations of the kidney as well as blood biochemistry. VCM administration resulted in a decrease of body weight and increase of kidney weight. Histological examination revealed renal damage such as dilated proximal tubules with occasional casts and interstitial fibrosis in VCM-treated mice. Furthermore, immunohistochemical staining with anti-CD10 and anti-single-stranded DNA antibodies highlighted damaged renal proximal tubules with marked dilatation as well as numerous apoptotic cells as early as day 4 of VCM-treatment. The severity of symptoms progressed until day 15. These results suggest that VCM-induced renal damage and incipient renal failure begin soon after the start of treatment and progressively worsen. This is the first report describing the time-dependence of VCM-induced nephrotoxicity in mice and depicting a model that clarifies the mechanisms of this tissue damage.</p>

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