![Sample our Bioscience journals, sign in here to start your access, Latest two full volumes FREE to you for 14 days]({"type":"image" , "src" : "/sda/5925/TOC-Subject-Sample-2021-Bioscience.jpg"})
Abstract
Interstitial fibrosis (IF) and tubular atrophy (TA) are integral parts of chronic allograft dysfunction and represent in the new classification a separate entity with or without the identification of a specific etiology. Loss of kidney graft function with IF/TA is one of the causes of most kidney allograft losses. Despite progress in immunosuppression, chronic allograft dysfunction remains the main clinical challenge for improving long-term graft survival. The sustained damage to the allograft does not represent a single entity but the summated effects of tissue injury from several pathogenic insults, as well as the kidney’s healing response, modified by alloimmunity and immunosuppression. A major challenge in the future of kidney transplantation includes the study of chronic allograft dysfunction pathogenesis to identify early markers of disease progression, as well as potential therapeutics pathways.
Financial & competing interests disclosure
The research results included in this report were partially supported by a National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) grant, R01DK080074. The authors declare that they have no competing interests. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.