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NDT Advance Access originally published online on November 5, 2007
Nephrology Dialysis Transplantation 2008 23(3):842-852; doi:10.1093/ndt/gfm694
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury

Gang Jee Ko, Chang-Su Boo, Sang-Kyung Jo, Won Yong Cho and Hyoung Kyu Kim

Division of Nephrology, Department of Internal Medicine, College of Medicine, Korea University, Institute of Renal disease, Seoul, Korea

Won Yong Cho, Division of Nephrology, Department of Internal Medicine, 5Ka, Anam-Dong, Sungbuk-Ku, Korea University Hospital, Seoul, Korea. Tel: + 82-2-920-5599; Fax: + 82-2-927-5344; E-mail: wonyong{at}korea.ac.kr



  Abstract

Background. Ischaemia/reperfusion is a major cause of acute kidney injury and can result in poor long-term graft function. Although most of the patients with acute kidney injury recover their renal function, significant portion of patients suffer from progressive deterioration of renal function. A persistent inflammatory response might be associated with long-term changes following acute ischaemia/reperfusion. Macrophages are known to infiltrate into tubulointersitium in animal models of chronic kidney disease. However, the role of macrophages in long-term changes after ischaemia/reperfusion remains unknown. We aimed to investigate the role of macrophages on the development of tubulointerstitial fibrosis and functional impairment following acute ischaemia/reperfusion injury by depleting macrophages with liposome clodronate.

Methods. Male Sprague–Dawley rats underwent right nephrectomy and clamping of left renal vascular pedicle or sham operation. Liposome clodronate or phosphate buffered saline was administered for 8 weeks. Biochemical and histological renal damage and gene expression of various cytokines were assessed at 4 and 8 weeks after ischaemia/reperfusion.

Results. Ischaemic/reperfusion injury resulted in persistent inflammation and tubulointerstital fibrosis with decreased creatinine clearance and increased urinary albumin excretion at 4 and 8 weeks. Macrophage depletion attenuated those changes. This beneficial effect was accompanied with a decrease in gene expression of inflammatory and profibrotic cytokines.

Conclusions. These results suggest that macrophages play an important role in mediating persistent inflammation and fibrosis after ischaemia/reperfusion leading to a development of chronic kidney disease. Strategies targeting macrophage infiltration or activation can be useful in the prevention of development of chronic kidney disease following ischaemic injury.

Keywords: acute renal failure; fibrosis; inflammation; ischaemia/reperfusion; long-term effect; macrophage

Received for publication: 23. 5.07
Accepted in revised form: 7. 9.07


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