In addition to these shared pathways, CKD may also potentiate the effects of hyperglycemia on PaC development as exogenous or endogenous uremic toxins, angiotensin II, iron overload, and lipoperoxides create substantial amount of reactive oxygen species, which in turn upregulates advanced glycation products receptors expression via inhibition of glyceraldehyde-3-phosphate dehydrogenase and accumulation of upstream glycolytic intermediates [40, 41]. The gene discussed is GAPDH; the disease is Hyperglycemia.