Tubular expression of KIM-1 does not predict delayed function after transplantation
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, 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
Abstract
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.
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Source: PubMed