Objective To establish an animal model of Kümmell disease ( KD) characterized by kidney deficiency and blood stasis, providing a foundation for exploring therapeutic targets and underlying pathophysiological mechanisms. Methods Forty SD rats were randomly assigned to normal, osteoporosis ( OP ), sham operation ( Sham), control, and model(KD) groups. Rats in the KD group underwent ovariectomy to induce kidney deficiency,followed 2 months later by creation of coccygeal bone defects and application of mechanical stress for 4 weeks. One week after bone defect surgery, subcutaneous injections of adrenaline hydrochloride were administered to induce blood stasis. Control group rats underwent ovariectomy and bone defect surgery but received 0. 9% sodium chloride solution.During the experiment, body temperature, body mass, food and water intake, and tongue characteristics were monitored. After model establishment, behavioral assessments, imaging analyses, hemorheological testing, and histopathological examinations were performed. Results Compared with the sham and control groups, KD group rats showed elevated body temperature, mass loss, reduced food intake, purple tongues with tortuous sublingual veins, dry fur, lethargy, and impaired mobility. Imaging revealed cortical thinning, sparse and fractured trabeculae, and vacuum cleft signs in vertebral bodies. Hemorheological evaluation showed significantly increased whole blood viscosity at low, medium, and high shear rates, increased plasma viscosity, elevated fibrinogen levels, and shortened thrombin time, prothrombin time, and activated partial thromboplastin time. Serum calcium and phosphorus levels decreased, while bone turnover markers increased. Thyroid hormone and estradiol levels were significantly lower than in the sham group. Histopathological examination showed KD group disrupted trabecular structure and reduced new bone formation compared with the control group. Conclusions Combined ovariectomy, adrenaline-induced blood stasis, and mechanical stress successfully establish a rat model of KD with kidney deficiency and blood stasis syndrome, providing a useful platform for mechanistic studies and therapeutic evaluation.