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NDT Advance Access originally published online on March 30, 2006
Nephrology Dialysis Transplantation 2006 21(7):1773-1775; doi:10.1093/ndt/gfl141
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Translational Nephrology

A Crry for polar shedding

Comments on Thurman JM, Ljubanovic D, Royer PA et al. Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischaemia/reperfusion. J Clin Invest 2006; 116:357–368

Masaomi Nangaku

Division of Nephrology and Endocrinology, University of Tokyo School of Medicine

Correspondence and offprint requests to: Dr Masaomi Nangaku, Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, 7-3-1, Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. Email: mnangaku-tky@umin.ac.jp

Keywords: acute kidney failure; complement regulatory protein; Crry; cytoskeleton; ischaemia

The first 10% of the full text of this article appears below.

Renal ischaemia plays a crucial role in the pathogenesis of acute renal failure. This ischaemia is also the primary factor in radio-contrast nephropathy, kidney transplantation and the progression of various kinds of chronic kidney diseases.

Ischaemic renal failure is associated with the loss of tubular epithelial cell polarity [1,2]. This change in cell polarity has multiple functional sequelae which result from the subsequent incorrect targeting of membrane proteins. Sodium/potassium-ATPase, for example, which is usually confined to the basolateral domain, is misdirected to the apical membrane, resulting in impaired transcellular sodium transport. Misdirected targeting of integrins, which anchor epithelial cells to extracellular matrix, causes viable tubular epithelial . . . [Full Text of this Article]


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