By integrating network pharmacology and spatially resolved metabolomics, potential PM-D nephrotoxic mechanisms were related to oxidative stress caused by metabolic disorders, such as in α-linolenic acid and linoleic acid metabolism, carnitine synthesis, fatty acid oxidation, and pyrimidine metabolism, which potentially caused apoptosis via PI3K-AKT pathway inhibition by regulating BCL2 and HSP90 targets. The gene discussed is BCL2; the disease is metabolic disease.