As hyperglycemia among diabetic patients induces podocyte injury as well as endothelial cell and tubulointerstitial injury through the formation of advanced glycation end‐products (AGE), activation of protein kinase C (PKC) and generation of reactive oxygen species, this process plays a pivotal role in initiation and progression of proteinuria and diabetic nephropathy[34]. This evidence concerns the gene PRRT2 and diabetic kidney disease.