Advanced glycation end products (AGEs) trigger various metabolic diseases and accumulate in the organs during the onset of metabolic diseases. The AGE-receptor for AGE (RAGE) interactions are strongly associated with the onset of chronic renal disease and diabetic nephropathy. This study evaluated the effects of glyoxal-lysine dimer (GOLD) and methylglyoxal-lysine dimer (MOLD) accumulation on various mechanisms in SV40 MES 13 kidney cells, which are currently unclear. GOLD and MOLD showed different effects on oxidative stress, inflammation, mitochondrial dysfunction, autophagy, and apoptosis. GOLD did not induce cytotoxicity or interact with RAGE. By contrast, MOLD significantly reduced the cell viability and interacted with RAGE. This study tested whether the RAGE interaction could cause differences in the effects of GOLD and MOLD on the mechanisms studied. GOLD did not generate oxidative stress or interact with RAGE and did not show toxicity through other mechanisms. Nevertheless, MOLD caused oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis, which are representative glucotoxicity mechanisms of AGE-RAGE interactions, and autophagy. Overall, these findings suggest that AGEs may show different toxicities in various organs. GOLD accumulation in the kidneys might not affect disease occurrence, but MOLD accumulation can promote disease.