Return to Medical Devices Alert Section
Data from Korea University advance knowledge in acute ischaemia
April 28th, 2008
2008 APR 28 -- "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," scientists in Seoul, South Korea report. "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. 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. 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. 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," wrote G.J. Ko and colleagues, Korea University. The researchers concluded: "Strategies targeting macrophage infiltration or activation can be useful in the prevention of development of chronic kidney disease following ischaemic injury." Ko and colleagues published their study in Nephrology Dialysis Transplantation (Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury. Nephrology Dialysis Transplantation, 2008;23(3):842-852). For additional information, contact W.Y. Cho, Korea University, Division Nephrology, Dept. of Internal Medical, College Medical, Institute Renal Diseases, 5Ka, Anam Dong, Seoul 136701, South Korea. The publisher's contact information for the journal Nephrology Dialysis Transplantation is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England. Keywords: South Korea, Seoul, Acute Ischaemia, Acute Kidney Failure, Acute Renal Failure, Antihypocalcemic, Antineoplastic, Biotechnology, Bisphosphonate, Blood Transfusion, Clodronate, Dialysis, Fibrosis, Gene Therapy, Hepatology, Inflammation, Ischemia-Reperfusion Injury, Kidney, Kidney Disease, Medical Device, Nephrectomy, Nephrology, Osteoporosis Prophylactic, Perfusion, Renal Failure, Renal Function, Reperfusion, Surgery, Transfusion Medicine, Transplantation, Korea University. This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2008, Biotech Business Week via NewsRx.com.
Return to Medical Devices Alert Section
|
