Our patient showed no evidence of clinical shock or tissue hypoperfusion upon presentation, except for the findings consistent with ATN, suggesting metformin as the major contributing cause of lactic acidosis. The presence of an angiotensin-converting enzyme inhibitor interfering with autoregulation at the level of the renal arteriole in the setting of volume depletion is a plausible explanation for the development of ATN in our case. This evidence concerns the gene ACE and lactic acidosis.