Moreover, the proximal tubule is thought to make little use of reabsorbed glucose under normal conditions, but acute kidney injury may induce a relevant glycolytic shift in the outer medullary proximal tubules,19,20 an effect that could involve the tubular upregulation of HIF-1α.21 Whether the increased delivery of glucose to this region of the kidney via SGLT2 inhibition is detrimental or beneficial in conditions of acute kidney injury remains to be determined. Here, HIF1A is linked to acute kidney injury.