The Met receptor tyrosine kinase is known to play an important role in renal repair after Acute Kidney Injury (AKI). We find that energetic stress induces rapid dephosphorylation of the Met RTK, and the Met ligand, HGF, blocks stress-induced loss of Met activity. This suggests that early HGF addition could enhance signaling for renal repair during energetic stress from AKI. Understanding the mechanisms involved may lead to interventions for improved patient recovery from AKI.