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01.12.2014 | Review | Ausgabe 1/2014 Open Access

Fibrogenesis & Tissue Repair 1/2014

Recent advances in renal interstitial fibrosis and tubular atrophy after kidney transplantation

Zeitschrift:
Fibrogenesis & Tissue Repair > Ausgabe 1/2014
Autoren:
Xiaojun Li, Shougang Zhuang
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1755-1536-7-15) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

XL wrote and revised the manuscript; SZ wrote and edited the manuscript. Both authors read and approved the final manuscript.

Abstract

Although kidney transplantation has been an important means for the treatment of patients with end stage of renal disease, the long-term survival rate of the renal allograft remains a challenge. The cause of late renal allograft loss, once known as chronic allograft nephropathy, has been renamed “interstitial fibrosis and tubular atrophy” (IF/TA) to reflect the histologic pattern seen on biopsy. The mechanisms leading to IF/TA in the transplanted kidney include inflammation, activation of renal fibroblasts, and deposition of extracellular matrix proteins. Identifying the mediators and factors that trigger IF/TA may be useful in early diagnosis and development of novel therapeutic strategies for improving long-term renal allograft survival and patient outcomes. In this review, we highlight the recent advances in our understanding of IF/TA from three aspects: pathogenesis, diagnosis, and treatment.
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