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. 2016 Mar;30(3):218-25.
doi: 10.1111/ctr.12677. Epub 2016 Jan 30.

EMMPRIN expression is involved in the development of interstitial fibrosis and tubular atrophy in human kidney allografts

Stephan Kemmner  1 , Christian Schulte  1 , Claus Hann von Weyhern  2 , Roland Schmidt  3 , Marcus Baumann  1 , Uwe Heemann  1 , Lutz Renders  1 , Christoph Schmaderer  1
Affiliations

EMMPRIN expression is involved in the development of interstitial fibrosis and tubular atrophy in human kidney allografts

Stephan Kemmner et al. Clin Transplant. 2016 Mar.

Abstract

Background: Matrix metalloproteinases (MMP) are involved in the development of interstitial fibrosis and tubular atrophy (IF/TA) in renal disease. The synthesis of MMP is activated by the extracellular matrix metalloproteinases inducer protein (EMMPRIN). To analyze the role of EMMPRIN in IF/TA, we retrospectively detected EMMPRIN expression in specimens of human renal allografts with various levels of IF/TA.

Methods: Immunohistochemistry was performed to detect EMMPRIN expression. In a retrospective analysis, a total cohort of 50 specimens were divided according to BANFF-classification into four subgroups (0-3): no, mild (≤ 25%), moderate (26-50%), or severe (>50%) IF/TA. Among other parameters, renal function was analyzed and compared to EMMPRIN expression.

Results: In 24 of 38 biopsies, we detected positive EMMPRIN staining. All nephrectomy (n = 12) samples were negative for EMMPRIN. Positive staining in the biopsy samples was detectable on the basolateral side of tubular epithelial cells. EMMPRIN staining was negatively correlated with IF/TA (p < 0.001). We found significant differences between the mean EMMPRIN expression in IF/TA groups 0 and 3 (p = 0.021) and groups 1 and 3 (p = 0.004). Furthermore, we found significant correlations between EMMPRIN staining and renal function.

Conclusion: Our data suggest that EMMPRIN is involved in the pathophysiology of IF/TA.

Keywords: CD147/basigin; chronic allograft dysfunction; extracellular matrix metalloproteinases inducer; interstitial fibrosis and tubular atrophy; kidney transplantation; matrix metalloproteinases.

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