Abstract
Interstitial fibrosis with tubule atrophy (IF/TA) is the response to virtually any sustained kidney injury and correlates inversely with kidney function and allograft survival. IF/TA is driven by various pathways that include hypoxia, renin-angiotensin-aldosterone system, transforming growth factor-β signaling, cellular rejection, inflammation, and others. In this review, we will focus on key pathways in the progress of renal fibrosis, diagnosis and therapy of allograft fibrosis. This review discusses the role and origin of myofibroblasts as matrix producing cells and therapeutic targets in renal fibrosis with a particular focus on renal allografts. We summarize current trends to use multiomic approaches to identify new biomarkers for IF/TA detection and to predict allograft survival. Furthermore, we review current imaging strategies that might help to identify and follow-up IF/TA complementary or as alternative to invasive biopsies. We further discuss current clinical trials and therapeutic strategies to treat kidney fibrosis.
| Original language | English |
|---|---|
| Pages (from-to) | E114-E130 |
| Journal | Transplantation |
| Volume | 105 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - Oct 2021 |
Bibliographical note
Funding Information:This work was supported by the START-Program of the Faculty of Medicine, RWTH Aachen (21/20, T.S.); the Else Kröner-Fresenius Stiftung (2015_A197, T.S.); and the Clinician-Scientist program of the German Society of Internal Medicine (T.S.). R.K. received support from grants of the German Research Foundation (DFG: SFBTRR57, SFBTRR219, CRU344, and SCHN 1188/5-1); a grant of the State of North Rhine-Westphalia (Return to NRW); a grant of the ERA-CVD (MEND-AGE), the Dutch Kidney Foundation (TASKFORCE), the BMBF eMed Consortia Fibromap, the Else Kroener Fresenius Foundation (CureStenosis); and a grant of the Interdisciplinary Centre for Clinical Research (IZKF) within the faculty of Medicine at RWTH Aachen University (O3-11).
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