Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Schröppel, B. et al.

Bernd Schröppel, Bernd Krüger, Liron Walsh, Melissa Yeung, Shay Harris, Krista Garrison, Jonathan Himmelfarb, Susan M. Lerner, Jonathan S. Bromberg, Ping L. Zhang, Joseph V. Bonventre, Zhu Wang, Alton B. Farris, Robert B. Colvin, Barbara T. Murphy, John P. Vella,

Tubular expression of KIM-1 does not predict delayed function after transplantation.

Injured epithelial cells of the proximal tubule upregulate the glycoprotein kidney injury molecule 1 (KIM-1), suggesting its potential as a biomarker of incipient kidney allograft injury. It is unknown whether KIM-1 expression changes in kidney allografts with delayed graft function (DGF), which often follows ischemia-reperfusion injury. Here, we prospectively measured KIM-1 RNA and protein expression in preperfusion biopsies of 30 living- and 85 deceased-donor kidneys and correlated the results with histologic and clinical outcomes after transplantation. We detected KIM-1 expression in 62% of deceased-donor kidneys and only 13% of living-donor kidneys (P < 0.0001). The level of KIM-1 expression before reperfusion correlated inversely with renal function at the time of procurement and correlated directly with the degree of interstitial fibrosis. Surprising, however, we did not detect a significant correlation between KIM-1 staining intensity and the occurrence of DGF. Our findings are consistent with a role for KIM-1 as an early indicator of tubular injury but do not support tissue KIM-1 measurement before transplantation to identify kidneys at risk for DGF.[1]

References

Tubular expression of KIM-1 does not predict delayed function after transplantation. Schröppel, B., Krüger, B., Walsh, L., Yeung, M., Harris, S., Garrison, K., Himmelfarb, J., Lerner, S.M., Bromberg, J.S., Zhang, P.L., Bonventre, J.V., Wang, Z., Farris, A.B., Colvin, R.B., Murphy, B.T., Vella, J.P. J. Am. Soc. Nephrol. (2010) [Pubmed]

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