Tags

Type your tag names separated by a space and hit enter

Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury.
Nephrol Dial Transplant. 2008 Mar; 23(3):842-52.ND

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.

Authors+Show Affiliations

Division of Nephrology, Department of Internal Medicine, College of Medicine, Korea University, Seoul, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17984109

Citation

Ko, Gang Jee, et al. "Macrophages Contribute to the Development of Renal Fibrosis Following Ischaemia/reperfusion-induced Acute Kidney Injury." Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, vol. 23, no. 3, 2008, pp. 842-52.
Ko GJ, Boo CS, Jo SK, et al. Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury. Nephrol Dial Transplant. 2008;23(3):842-52.
Ko, G. J., Boo, C. S., Jo, S. K., Cho, W. Y., & Kim, H. K. (2008). Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury. Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, 23(3), 842-52.
Ko GJ, et al. Macrophages Contribute to the Development of Renal Fibrosis Following Ischaemia/reperfusion-induced Acute Kidney Injury. Nephrol Dial Transplant. 2008;23(3):842-52. PubMed PMID: 17984109.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury. AU - Ko,Gang Jee, AU - Boo,Chang-Su, AU - Jo,Sang-Kyung, AU - Cho,Won Yong, AU - Kim,Hyoung Kyu, Y1 - 2007/11/05/ PY - 2007/11/7/pubmed PY - 2008/4/24/medline PY - 2007/11/7/entrez SP - 842 EP - 52 JF - Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association JO - Nephrol Dial Transplant VL - 23 IS - 3 N2 - 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. SN - 1460-2385 UR - https://www.unboundmedicine.com/medline/citation/17984109/Macrophages_contribute_to_the_development_of_renal_fibrosis_following_ischaemia/reperfusion_induced_acute_kidney_injury_ L2 - https://academic.oup.com/ndt/article-lookup/doi/10.1093/ndt/gfm694 DB - PRIME DP - Unbound Medicine ER -