BMC Nephrology

official impact factor 2.14
Search for
Advanced search
BMC Nephrology
Tools
Share this article
Open Access Research article

Ozonated autohemotherapy: protection of kidneys from ischemia in rats subjected to unilateral nephrectomy

Chiara Foglieni1, Alessandro Fulgenzi2, Daniela Belloni3, Clara Sciorati4, Elisabetta Ferrero3 and Maria E Ferrero2*

Author Affiliations

1 Clinical Cardiovascular Biology Laboratory, San Raffaele Scientific Institute, Milano, Italy

2 Dipartimento di Morfologia Umana e Scienze Biomediche - Città Studi, Università degli Studi di Milano, Milan, Italy

3 Department of Oncology, IRCCS H San Raffaele, Milan, Italy

4 Laboratory of Lymphoid Malignancies, San Raffaele Scientific Institute, Milan, Italy

For all author emails, please log on.

BMC Nephrology 2011, 12:61 doi:10.1186/1471-2369-12-61

Published: 14 November 2011

Abstract

Background

Ozonated autohemotherapy (OA) has been previously successfully used in the treatment of patients affected by peripheral occlusive arterial disease. OA consists of an intrafemoral reinfusion of autologous blood previously exposed to a mixture of oxygen/ozone (O2/O3). This study analyzes the effects of OA in protecting rat kidney from ischemia and ischemia/reperfusion damage.

Methods

We performed OA 30 min before the induction of 60 min renal ischemia or at the induction of 60 min postischemic reperfusion in rats subjected to unilateral nephrectomy. In addition, to evidence the possible protection induced by O2/O3 on endothelial functions, the present study analyzes the in vitro effects of O2/O3 on oxygen consumption by human umbilical vein endothelial cells (HUVEC).

Results

1) OA preserves rat kidney functions and architecture, as demonstrated by the improved levels of serum creatinine and blood urea nitrogen and by histology; 2) such protection does not correlate with the increase of plasmatic nitric oxide, but is compatible with a focal renal increase of renal βNADPH-diaphorase; 3) treatment of HUVEC with O2/O3 significantly increases both the rate of oxygen consumption and the mitochondrial activity assessed by confocal microscopy.

Conclusion

The preservation of the mitochondrial activity of endothelium could in vivo limit the endothelial dysfunction provoked by the Isc or Isc/R processes.