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Comparative Study
. 2015 Feb 13:16:19.
doi: 10.1186/s12882-015-0011-y.

Kidney injury molecule-1 expression in human kidney transplants with interstitial fibrosis and tubular atrophy

Aline Lima Nogare  1 , Francisco Veríssimo Veronese  2   3 , Virna Nowotny Carpio  4 , Rosangela Munhoz Montenegro  5 , José Alberto Pedroso  6 , Karla Laís Pegas  7 , Luiz Felipe Gonçalves  8   9 , Roberto Ceratti Manfro  10   11
Affiliations
Comparative Study

Kidney injury molecule-1 expression in human kidney transplants with interstitial fibrosis and tubular atrophy

Aline Lima Nogare et al. BMC Nephrol. .

Abstract

Background: 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. 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.

Methods: Protein 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.

Results: KIM-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.

Conclusions: KIM-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.

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Figures

Figure 1
Figure 1
The dot-plot representation graphics showing the medians and distribution of the quantification levels of normalized KIM-1 mRNA (2 -ΔΔCT ) according to the Banff diagnostic groups. Panel A: kidney tissue. Panel B: urinary sediment cells. ATN = acute tubular necrosis; AR = acute rejection; CIN = calcineurin inhibitor-induced nephrotoxicity; IFTA = interstitial fibrosis and tubular atrophy.
Figure 2
Figure 2
Immunohistochemical staining of KIM-1 in non-atrophic proximal tubules of kidney transplant for-cause biopsies according to staining intensity. Slide A: interstitial fibrosis and tubular atrophy, 3+; Slide B: acute tubular necrosis, 2+; Slide C; acute rejection, 1+; Slide D: calcineurin inhibitor nephrotoxicity, very weak staining (original magnification x 400 in A-D).
See this image and copyright information in PMC

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