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Published ahead of print on January 4, 2006
J Am Soc Nephrol 17: 368-377, 2006
© 2006 American Society of Nephrology
doi: 10.1681/ASN.2005080859
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Frontiers in Nephrology: Diabetic Nephropathy: Understanding Mechanism and Defining Risk

Leukocyte Recruitment and Vascular Injury in Diabetic Nephropathy

Elena Galkina and Klaus Ley

Department of Biomedical Engineering and Robert M. Berne Cardiovascular Research Center, University of Virginia, Health Sciences Center, Charlottesville, Virginia

Address correspondence to: Dr. Klaus Ley, Robert M. Berne Cardiovascular Research Center, University of Virginia, PO Box 801394, Charlottesville, VA 22908. Phone: 434-243-9966; Fax: 434-924-2828; Email: klausley{at}virginia.edu

Different types of activated leukocytes play a crucial role in the pathogenesis of most kidney diseases from acute to chronic stages; however, diabetic nephropathy was not considered an inflammatory disease in the past. This view is changing now because there is a growing body of evidence implicating inflammatory cells at every stage of diabetic nephropathy. Renal tissue macrophages, T cells, and neutrophils produce various reactive oxygen species, proinflammatory cytokines, metalloproteinases, and growth factors, which modulate the local response and increase inflammation within the diabetic kidney. Although the precise mechanisms that direct leukocyte homing into renal tissues are not fully identified, it has been reported that intercellular adhesion molecule-1 and the chemokines CCL2 and CX3CL1 probably are involved in leukocyte migration in diabetic nephropathy. This review focuses on the molecular mechanisms of leukocyte recruitment into the diabetic kidney and the involvement of immigrated immune cells in the damage to renal tissues.




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