Abstract
BackgroundKidney injury molecule-1 (KIM-1) is expressed in tubular epithelial cells after injury and may have a role in the development of renal graft fibrosis. In this study we evaluated the molecular and protein expressions of KIM-1 in dysfunctional allografts and also mRNA KIM-1 expression in urine as potential biomarkers of graft fibrosis.MethodsProtein and mRNA levels in renal tissue and urinary sediment cells of 69 kidney transplant recipients that undertook for-cause graft biopsies were evaluated by immunohistochemistry and real-time polymerase chain reaction. The histopathology was classified according to the 2007 Banff schema.ResultsKIM-1 protein expression was increased in biopsies with interstitial fibrosis and tubular atrophy (IF/TA) compared with biopsies showing acute calcineurin inhibitor nephrotoxicity (CIN) (P <0.05). Kidney tissue KIM-1 mRNA signaling (in) was increased in biopsies with IF/TA compared with all other groups (P <0.05). In the urine cells KIM-1 mRNA was also increased in patients with IF/TA compared with patients with acute CIN (P <0.05). Significant correlations were found between KIM-1 protein and mRNA levels in tissue, between mRNA expressions in tissue and urine and between protein tissue expression and gene expression in the urine.ConclusionsKIM-1 seems to be a marker of kidney graft fibrosis. Urinary KIM-1 mRNA may become a useful non-invasive biomarker of the injuries that can trigger intra-graft fibrotic processes, such as interstitial fibrosis and tubular atrophy.
Highlights
Kidney injury molecule-1 (KIM-1) is expressed in tubular epithelial cells after injury and may have a role in the development of renal graft fibrosis
A significantly higher serum creatinine was observed in the acute tubular necrosis (ATN) group as compared to the patients classified in the other groups (P
In the present study we found that, in the renal tissue of for cause kidney allograft biopsies, mRNA expression is paralleled by protein expression and that urinary sediment cells (USC) KIM-1 mRNA transcripts increases in parallel with protein expression
Summary
Kidney injury molecule-1 (KIM-1) is expressed in tubular epithelial cells after injury and may have a role in the development of renal graft fibrosis. A variety of injuries to the allograft shortens significantly transplant survival as demonstrated by currently observed half-lives, still much inferior desired [2]. These injuries lead to allograft fibrosis that is mainly. KIM-1 (kidney injury molecule-1) is a type 1 transmembrane glycoprotein not detectable in normal kidney tissue but inducible by ischemic and toxic insults. This protein expresses in elevated amounts in the apical surface of surviving proximal tubule epithelial cells and is detectable in the urine [5]. In our previous studies we found that KIM-1 messenger RNA, along with another fibrosis related molecules, to be augmented in renal allografts with fibrosis [7,8]
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