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NDT Advance Access originally published online on March 23, 2009
Nephrology Dialysis Transplantation 2009 24(11):3265-3268; doi:10.1093/ndt/gfp010
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© The Author 2009. Published by Oxford University Press [on behalf of ERA-EDTA]. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Kidney injury molecule-1 (KIM-1): a urinary biomarker and much more

Joseph V. Bonventre

Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA

Correspondence and offprint requests to: Joseph V. Bonventre; E-mail: joseph_bonventre@hms.harvard.edu

Keywords: acute kidney injury; TIM-1; acute renal failure; phagocytosis; apoptosis

The first 150 words of the full text of this article appear below.



   KIM-1 kidney expression and function
 
The kidney injury molecule-1 (designated as Kim-1 in rodents, KIM-1 in humans) mRNA was identified using techniques of representational difference analysis, a PCR-based technique [1], which we carried out to find genes whose expression was markedly upregulated 24–48 h after ischaemia in the rat [2]. Kim-1 was the gene found to be most highly upregulated in this screen. A large pharmaceutical company consortium, using an unbiased genomic approach to evaluate genes upregulated with the nephrotoxin cisplatin, determined that Kim-1 was upregulated more than any other of the 30 000 genes tested [3]. There are a large number of studies in animals showing robust Kim-1 protein production in the affected segments of the proximal tubule whenever a toxin or pathophysiological state results in dedifferentiation of the epithelium (e.g. [4–6]). Dedifferentiation is a very early manifestation of the epithelial cell response to injury [7. . . [Full Text of this Article]



   KIM-1 as a biomarker
 

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