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Quantitative Analyses of Kidney Injury Molecule-1 Messenger RNA in Kidney Transplant Recipients With Graft Dysfunction

Abstract Background Kidney injury molecule-1 (KIM-1), a type I transmembrane protein that is not expressed in normal renal tissue, shows increased expression in dedifferentiated cells within damaged regions of the proximal tubule. We evaluated mRNA transcription of the KIM-1 gene in renal tissue of...

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Published in:Transplantation proceedings 2010-03, Vol.42 (2), p.473-474
Main Authors: Nogare, A.L, Joelsons, G, Pedroso, J.A.R, Veronese, F.J.V, Gonçalves, L.F, Manfro, R.C
Format: Article
Language:English
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Summary:Abstract Background Kidney injury molecule-1 (KIM-1), a type I transmembrane protein that is not expressed in normal renal tissue, shows increased expression in dedifferentiated cells within damaged regions of the proximal tubule. We evaluated mRNA transcription of the KIM-1 gene in renal tissue of kidney transplant patients who were experiencing graft dysfunction searching for an accurate biomarker of kidney graft injury. Patients and Methods mRNA analysis was performed on 59 biopsies from kidney transplant patients who had been classified according to the Banff 1997 scheme. Biopsies were categorized in 5 diagnostic groups: acute tubular necrosis (ATN) with superimposed acute rejection episode (ARE), ATN; ARE; calcineurin inhibitor nephrotoxicity (CIN); or interstitial fibrosis and tubular atrophy (IFTA). Amplified tissue RNA was quantified by real-time polymerase chain reaction. Results Renal tissue evaluations showed significantly increased KIM-1 mRNA expression as shown by median values, 25–75 percentiles, and averages of the logaritmic transformation: namely, CIN group (50.6; 1.8–285, 1; 1.24) and IFTA group (7.5; 1.26–14.6; 0.62), displayed significant differences ( P > .05). In contrast, expression was lower among the ATN (0.47; 0.28–1.06; −0.13); ARE (0.21; 0.11–0.78; −0.45), and ATN+ARE (0.46; 0.06–3.27; −0.25) cohorts. Conclusion These preliminary data suggested that KIM-1 mRNA might be useful biomarker of tubular damage associated with CIN and IFTA.
ISSN:0041-1345
1873-2623
DOI:10.1016/j.transproceed.2010.01.042