Acute kidney injury (AKI) remains a frequent complication of severe disease. Despite progress in supportive care, the overall mortality and long-term consequences of this complication have not changed significantly. Although complex genetic models and cell lineage tracking have identified subsets of cells that play a central role during the recovery of renal function, the processes that occur immediately after an injury remain unknown because it is virtually impossible to assess these events in mammalian models. We now established an approach to elucidate early adaptive changes after kidney damage at the molecular level. Extracting key regulators that orchestrate adaptive responses, we are translating experimental observations into clinical applications.

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