Reduction of renal fibrosis as a result of liposome encapsulated clodronate induced macrophage depletion after unilateral ureteral obstruction in rats

Nephron Exp Nephrol. 2007;105(1):e1-9. doi: 10.1159/000096859. Epub 2006 Nov 9.

Abstract

Background/aim: Macrophages have been thought to play a role in renal tubulointerstitial fibrosis; recent reports have demonstrated an antifibrotic effect of macrophages in late-stage renal fibrosis. Liposome-encapsulated clodronate (LC) produces a selective and systemic depletion of phagocytic macrophages in vivo. To study the role of initial infiltrating macrophages in renal fibrosis, we compared the effects of pretreatment with LC and a liposome vehicle for control of the severity of renal fibrosis in a unilateral ureteral obstruction (UUO) rat model.

Methods: One day after a single intravenous injection of LC or liposome vehicle, the rats underwent UUO. Following 1, 5, and 14 days, the kidneys were examined to evaluate macrophage infiltration and renal fibrosis.

Results: LC depleted macrophages systemically and reduced renal fibrosis associated with UUO; this beneficial effect was accompanied by a decrease of transforming growth factor beta mRNA expression. The osteopontin expression was also reduced by pretreatment with LC.

Conclusion: Initial interstitial infiltration of macrophages contributes to tubulointerstitial fibrosis in UUO.

MeSH terms

  • Animals
  • Clodronic Acid / administration & dosage*
  • Fibrosis
  • Kidney / pathology*
  • Liposomes
  • Macrophages / drug effects
  • Macrophages / physiology*
  • Male
  • Osteopontin / analysis
  • Rats
  • Rats, Sprague-Dawley
  • Transforming Growth Factor beta / analysis
  • Ureteral Obstruction / complications*

Substances

  • Liposomes
  • Transforming Growth Factor beta
  • Clodronic Acid
  • Osteopontin