Peer-Reviewed Publication
Nat Rev Nephrol2026September 10, 2026Journal Article

Mechanisms of regeneration and maladaptive repair in acute kidney injury.

Tobias Seibt1,2, Konrad Hoeft3,4, Gideon J L Schaefer3,4, Adam Wahida1,5,6,7,8,9,10, Razelle Kurzrock11, Marcus Conrad1,12, Rafael Kramann13,14,15
1Institute of Metabolism and Cell Death, Helmholtz Zentrum München, Neuherberg, Germany.
2Transplant Center, University Hospital Munich, Ludwig-Maximilians-University (LMU), Munich, Germany.
3Department of Medicine 2 (Nephrology, Rheumatology, Clinical Immunology and Hypertension), Medical Faculty, RWTH Aachen University, Aachen, Germany.
4Center of Excellence in Nephrology, University Hospitals of Aachen, Cologne and Dusseldorf, Aachen, Germany.
5Clinical Division of Oncology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
6Molecular Signaling and Cell Death Unit, VIB-UGent Center for Inflammation Research, Flanders Institute for Biotechnology, Ghent, Belgium.
7Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
8Krantz Family Center for Cancer Research and Department of Medicine, Massachusetts General Hospital Cancer Center, Boston, MA, USA.
9Department of Medicine, Harvard Medical School, Boston, MA, USA.
10Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
11MCW Cancer Center, Medical College of Wisconsin, Milwaukee, WI, USA.
12Translational Redox Biology, Natural School of Sciences, Technical University of Munich, Garching, Germany.
13Department of Medicine 2 (Nephrology, Rheumatology, Clinical Immunology and Hypertension), Medical Faculty, RWTH Aachen University, Aachen, Germany. rkramann@gmx.net.
14Center of Excellence in Nephrology, University Hospitals of Aachen, Cologne and Dusseldorf, Aachen, Germany. rkramann@gmx.net.
15Department of Internal Medicine, Nephrology and Transplantation, Erasmus Medical Center, Rotterdam, The Netherlands. rkramann@gmx.net.

Abstract

Acute kidney injury (AKI) is a major risk factor for the subsequent development and progression of chronic kidney disease (CKD), particularly when kidney repair is incomplete or maladaptive. The repair trajectory after kidney injury is primarily determined through the interconnected responses of tubular epithelial cells (TECs), immune cells and fibroblasts. Within this network, TECs act as sentine…

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