Diabetes is associated with a number of side effects including retinopathy, neuropathy, nephropathy and hypertension. Recent evidence has shown that serum and glucocorticoid regulated kinase-1 (SGK1) is increased in models of diabetic nephropathy. While clearly identified as glucocorticoid responsive, SGK1 has also been shown to be acutely regulated by a variety of other factors. These include insulin, hypertonicity, glucose, increased intracellular calcium and transforming growth factor-beta, all of which have been shown to be increased in type II diabetes. The principal role of SGK1 is to mediate sodium reabsorption via its actions on the epithelial sodium channel (now known as sodium channel, nonvoltage-gated 1). Small alterations in the sodium resorptive capacity of the renal epithelia may have dramatic consequences for fluid volume regulation, and SGK1 maybe responsible for the development of hypertension associated with diabetes. This short commentary considers the evidence that supports the involvement of SGK1 in diabetic hypertension, but also discusses how aberrant sodium reabsorption may account for the cellular changes seen in the nephron.