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

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 re...

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Veröffentlicht in:Clinical transplantation 2016-03, Vol.30 (3), p.218-225
Hauptverfasser: Kemmner, Stephan, Schulte, Christian, Hann von Weyhern, Claus, Schmidt, Roland, Baumann, Marcus, Heemann, Uwe, Renders, Lutz, Schmaderer, Christoph
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Sprache:eng
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Zusammenfassung: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.
ISSN:0902-0063
1399-0012
DOI:10.1111/ctr.12677