Objective To develop an animal model for Kümmell"s disease (KD) characterized by kidney deficiency and blood stasis, thereby facilitating the exploration of therapeutic targets and underlying mechanisms. Methods Twenty-four Sprague-Dawley rats were randomly allocated into three groups: sham operation, control, and model. The model group underwent ovariectomy to induce kidney deficiency, followed two months later by coccygeal bone defect creation and application of mechanical stress for four weeks. One week post-bone defect surgery, subcutaneous adrenaline hydrochloride injections were administered to induce blood stasis. The control group received ovariectomy and bone defect surgeries with normal saline injections. Throughout the experiment, body temperature, weight, food and water consumption, and tongue characteristics were monitored. Post-modeling, behavioral assessments, imaging analyses, hemorheological tests, and histopathological examinations were conducted. Results Compared to the sham and control groups, the model group exhibited elevated body temperatures, weight loss, reduced food intake, purple tongues with tortuous sublingual veins, dry fur, lethargy, and movement disturbances. Imaging revealed cortical thinning, sparse and fractured trabeculae, and vacuum cleft signs in the vertebral bodies of the model group. Hematologically, significant increases in whole blood viscosity (at low, medium, and high shears) and plasma viscosity, elevated fibrinogen levels, and shortened thrombin time, prothrombin time, and activated partial thromboplastin time were observed. Serum calcium and phosphorus levels decreased, while bone turnover markers increased. Thyroid hormone and estradiol levels were notably lower in the model group relative to the sham group. Histologically, the model group displayed disrupted trabecular architecture and reduced new bone compared to control. Conclusions Combining ovariectomy, adrenaline induction, and mechanical stress successfully establishes a rat model of KD with concurrent kidney deficiency and blood stasis syndrome, providing a platform for investigating therapeutic strategies and pathophysiological mechanisms.