PRRT2 and diabetic kidney disease: In addition to oxidative stress, renal cell injury in DKD mainly includes 4 pathogenic mechanisms: activation of polyol metabolic bypass, generation of Advanced Glycation End products and activation of their receptors (AGEs-RAGEs), activation of protein kinase C (PKC), and overactivation of hexosamine bypass.[22] However, clinical studies have found that blocking either of the above mechanisms of action alone is not effective in blocking the progression of DM (diabetes mellitus) microangiopathy .