A total of 20 healthy SPF male BALB/C mice aged 6－8 weeks were randomly divided into control group and model group， with 10 mice in each group. The IgAN model was constructed by the combined administration of bovine serum albumin （BSA）， lipopolysaccharide （LPS）， and carbon tetrachloride （CCl₄）.IgA deposits in glomeruli were detected by immunofluorescence method， and hematoxylin-eosin （HE） staining was used to observe the pathomorphology of kidney tissue of the mice to evaluate whether the model was successfully constructed.The body weights and kidney weights of the mice were weighed， and the kidney index was caculated.The levels of serum creatinine and urea nitrogen of the mice were detected by enzyme activity method.The levels of tumor necrosis factor-α （TNF-α）， interleukin 1-β （IL-1β） and interleukin 6 （IL-6） in serum of the mice in each group were detected by enzyme-linked immunosorbent assay （ELISA）. Real-time fluorescence quantitative polymerase chain reaction （RT-qPCR） was used to detect the mRNA expression levels of the key genes that regulated mitochondrial fission and fusion， including dynamic related protein 1 （Drp1）， mitofusin 1 （Mfn1） and mitofusin 2 （Mfn2）. The expression levels of Drp1， Mfn1， and Mfn2 proteins in kidney tissue of the mice were detected by Western blotting method.

Compared with control group， the glomerulus of the mice in model group showed that IgA deposition was obvious， accompanyied by glomerular atrophy， the hyperplasia of glomerular mesangial cells and stroma led to widening of the mesangial area， and a portion of renal tubule cells presented swelling and necrosis， indicating that the IgAN model was successfully constructed. Compared with control group， the kidney index and the serum creatinine and urea nitrogen levels of the mice in model group were obviously increased（P<0.05），the levels of serum TNF-α， IL-1β and IL-6 of the mice were increased significantly（P<0.05 or P<0.01），the expression levels of Drp1 mRNA and protein in kidney tissue of the mice were obviously increased（P<0.05）， while the expression levels of Mfn1 and Mfn2 mRNA and proteins in kidney tissue of the mice were obviously reduced（P<0.05）.

The imbalance of mitochondrial fission/fusion protein expression may be one of the mechanisms of the development and progression of IgAN， and the research of fission and fusion homeostasis as a target may provide new ideas for the therapy of IgAN.