Our observation that DG metabolism in the circulation was disturbed, with a higher correlation to clinical outcomes, may argue that a dysregulated DG-PKC/PKD signalling network could disrupt the redox balance and lead to more oxidative stress [53], and in part could explain why DSA-T2DM patients are more vulnerable to diabetic nephropathy progression. Here, PRKD1 is linked to type 2 diabetes mellitus.