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NDT Advance Access originally published online on September 3, 2008
Nephrology Dialysis Transplantation 2008 23(11):3394-3396; doi:10.1093/ndt/gfn480
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Kim-1/Tim-1: from biomarker to therapeutic target?*

Andrew J. Rees and Renate Kain

Institute of Clinical Pathology, Medical University of Vienna, Vienna, Austria

Correspondence and offprint requests to: Andrew J. Rees, Institute of Clinical Pathology, Medical University of Vienna, 18-20 Währinger Gürtel, A-1090 Vienna, Austria. Tel: +43-140400-3681; Fax: +43-140400-5193; E-mail: andrew.rees@meduniwien.ac.at

Keywords: acute kidney injury; apoptosis; Kim-1; phosphidylserine receptor

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

The best biomarkers turn out to be important in pathogenesis and some become therapeutic targets—a paradigm illustrated beautifully by the herceptin receptor in breast cancer [1]. A paper in the May issue of the Journal of Clinical Investigation raises the exciting possibility that the renal biomarker, kidney injury molecule-1 (Kim-1), may become an equally important example [2].

Kim-1 (also known as Tim-1—T-cell immunoglobulin and mucin-containing molecule) was originally discovered in a screen for molecules involved in the pathogenesis of acute kidney injury (AKI) [3]. Although undetectable in normal rat kidney, Kim-1 is abundantly expressed by proliferating and dedifferentiated renal proximal tubular epithelial cells 48 h after acute ischaemic injury in kidneys examined by in situ hybridization and immunohistochemistry. The human orthologue was also identified and behaved identically. The authors concluded that ‘Kim-1 may play an important role in the restoration of . . . [Full Text of this Article]


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