Objective: To explore the protective effects and underlying molecular mechanisms of Hexavitamin Soya Lecithin (HexaV) against alcohol-related renal injury. Methods: Specific pathogen-free (SPF) male C57BL/6 mice were randomly divided into three groups: control group (NC), alcohol-induced injury model group (ETOH), and HexaV treatment group (ETOH+HexaV). Renal pathological changes were evaluated by hematoxylin-eosin (H&E), Masson’s trichrome and periodic acid-Schiff (PAS) staining. Transcriptomic sequencing was performed on kidney tissues, and the mRNA expression levels of selected target genes were further validated by quantitative real-time polymerase chain reaction (qPCR). Results: After eight weeks of alcohol gavage, compared with the NC group, H&E staining of kidney tissues in the ETOH group revealed glomerular atrophy, mesangial proliferation, interstitial inflammatory cell infiltration, and vacuolar degeneration of renal tubular epithelial cells. Masson’s trichrome staining showed obvious blue collagen deposition, while PAS staining demonstrated thickened magenta-stained basement membrane structures. All these pathological changes were significantly alleviated by HexaV treatment. Transcriptomic sequencing identified 27 overlapping differentially expressed genes between the ETOH and ETOH+HexaV groups. KEGG enrichment analysis indicated that chronic alcohol exposure predominantly activated the renin—angiotensin system (RAS), endocrine-and other factor-regulated calcium reabsorption, and the interleukin 17 (IL-17) signaling pathway. These pathways were significantly upregulated in the ETOH group but were completely reversed in the ETOH+HexaV group. qPCR further confirmed that, compared with the NC group, RAS-related genes (Agt, Ace2, Ren1, and Klk1b3) and IL-17 signaling pathway-related genes (IL17d, Mmp3, Mapk10, Jun, Rela, Cebpd, Mapk4, Cxcl2, Cxcl10, Lcn2, and Fosb) were significantly upregulated in the ETOH group, and all these changes were reversed following HexaV intervention. Conclusion: HexaV improves alcohol-induced renal tissue damage and dysfunction, and delays the progression of alcoholic nephropathy by reversing the inflammatory and hemodynamic pathways activated by chronic alcohol exposure.