SERPINA1 and acute kidney injury: The pathophysiologic relevance of renal tubular AAT gene induction is indicated by the following: i) renal cortical levels of NE decline during AKI, despite increased NE gene transcription (as expected from rising AAT levels); ii) NE is directly cytotoxic to proximal tubule cells; iii) AAT completely blocks NE cytotoxicity; and iv) AAT can also mitigate Fe mediated oxidant tubular cell attack, likely due to its anti-protease activity.