Objective To investigate the mechanism of Liangxue Tuizi Formula (LXTZF) in treating Henoch-Sch?nlein purpura nephritis (HSPN) with blood-heat pattern in rat models, focusing on its inhibition of galactose-deficient IgA1 (Gd-IgA1) production via the B-cell activating factor (BAFF)/proliferation-inducing ligand (APRIL) signaling pathway. Methods Sixty Wistar rats were randomly divided into groups. An HSPN model with blood-heat pattern was established. The rats were allocated into a blank control group (n=8), a model group (n=8), a prednisone group (5.4 mg/kg/d, n=8), and three LXHZF groups – low-, medium-, and high-dose (3.8, 7.5, and 15.0 g/kg/d). Interventions were administered continuously for 4 weeks. Drug efficacy was evaluated by measuring 24-hour urinary protein, urinary red blood cells, histopathological changes, and molecular biological indicators. Results Compared with the blank control group, the model group showed significant increases in urinary protein, urinary red blood cells, serum levels of IgA1, Gd-IgA1, BAFF, APRIL, and renal circulating immune complexes (CIC) (P<0.05), along with evident renal pathological damage. All treatment groups effectively ameliorated these indicators. Notably, the medium- and high-dose LXTZF groups significantly downregulated the gene and protein expression levels of key molecules in the renal BAFF/APRIL signaling pathway, including BAFF, APRIL, and their receptors BAFFR, BCMA, and TACI. Conclusion Liangxue Tuizi Formula may alleviate skin and renal injury in HSPN rats with blood-heat pattern by suppressing the BAFF/APRIL signaling pathway, thereby reducing the generation of Gd-IgA1 and the deposition of immune complexes.