Abstract： Objective： To analyze the action mechanism of Kangfengshi Prescription in treating chronic glomerulonephritis （CGN） based on network pharmacology and molecular docking techniques. Methods： Active components and targets of Kangfengshi Prescription were collected using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform（TCMSP）. CGN disease targets were constructed using the GeneCards， PharmGkb， and OMIM databases. A "Chinese medicine-compound-target" network was constructed by Cytoscape software， and the intersection of potential targets of Kangfengshi Prescription and disease targets was obtained to identify core targets. A protein-protein interaction（PPI） network was constructed by the STRING platform； Gene Ontology（GO）functional and Kyoto Encyclopedia of Genes and Genomes（KEGG）pathway enrichment analyses of core targets were performed by bioinformatics resource databases， and constructed a "target-signaling pathway" core pathway map. Molecular docking was used to verify the binding ability of predicted targets and active components. Results：A total of 105 CGN disease targets were identified for Kangfengshi Prescription，with core targets including interleukin（IL）-6，tumor necrosis factor（TNF），chemokine ligand 2（CCL2），IL-1β，nuclear factor（NF）-κB p65 subunit（RELA）， protein kinase B1（AKT1）， tumor protein p53（TP53）， estrogen receptor α（ESR1）， transcription factor AP-1 subunits JUN and FOS. GO functional analysis mainly involved responses to lipopolysaccharide， bacterial molecules， reactive oxygen species， and oxidative stress； KEGG pathway enrichment mainly involved phosphatidylinositol 3-kinase（PI3K）-protein kinase B（AKT）， advanced glycation end productsreceptor （AGE-RAGE） in diabetic complications， mitogen-activated protein kinase （MAPK）， and lipid and atherosclerosis signaling pathways. Molecular docking showed good binding activity between core targets and core active components. Conclusion： Kangfengshi Prescription can treat CGN through active components such as quercetin and kaempferol acting on targets like TP53 and AKT1，and through signaling pathways such as PI3K-AKT，AGE-RAGE in diabetic complications，MAPK，and lipid and atherosclerosis.