LCN2 and acute kidney injury: The potential of SGL2is to inflict AKI with selective hypoxic outer medullary injury is illustrated by increasing plasma and urinary NGAL on admission in patients with diabetes hospitalized with AKI, while the corresponding levels of kidney ischemia molecule (KIM)-1 (a marker of proximal tubular injury) remains comparable to those of other patients with diabetes hospitalized without AKI [47].