The persistence of the BP-lowering effects of SGLT-2 inhibition in CKD is yet to be fully understood, and possibilities include BP being more responsive to salt mobilization and/or removal in CKD, increased response to the possible beneficial effects of SGLT-2 inhibition on arterial stiffness, sympathetic system overactivity, oxidative stress and endothelial dysfunction [62] and/or augmentation of the effect of other antihypertensive medications [62]. This evidence concerns the gene SLC5A2 and endothelial dysfunction.