NOX4 and diabetic kidney disease: It is well established that the renal hypertrophy of the remnant kidney after the ablation of the other kidney is compensatory (adaptive/physiological) but not pathological [37] and this phenomenon is independent of calcineurin, transforming growth factor-β1, reactive oxygen species, NAD(P)H oxidase 4 and local RAS components [38], all of which are proved to be upregulated in diabetic nephropathy or in other forms of renal injury.