Objective To establish and evaluate a model of chronic obstructive pulmonary disease (COPD) combined with chronic kidney disease (CKD) in rats. Methods Forty SPF grade SD rats were randomly divided into Control group, COPD group, CKD group, and COPD combined with CKD model (COPD + CKD) group, with 10 rats in each group. The COPD rat model was prepared by cigarette smoke exposure combined with the bacterial drip method, the CKD rat model was established by adenine induction, and the COPD combined with CKD rat model was prepared by both method. Results After successful modeling, lung function indexes incluidng forced vital capacity ( FVC), forced expiratory volume in 0. 1 s (FEV_{0. 1} ), and FEV_{0. 1} / FVC were significantly reduced in the COPD + CKD group (P< 0. 01), and lung histopathology showed emphysematous changes with alveolar wall fracture and fusion as well as inflammatory cell infiltration. Serum Cr, BUN, and 24 h urine protein were significantly increased (P< 0. 01). Renal histopathology showed glomerular mesentery proliferation, basement membrane thickening, tubular dilatation, and interstitial fibrosis. The ultrastructure showed that glomerular capillary loops were partially closed, foot processes were fused, renal tubule mitochondria were fused and disintegrated, and lysosome was increased. Serum IL-6, IL-13, IL-1β, and TGF-β1 levels were significantly increased (P< 0. 01) and were significantly higher than those in single model groups (P< 0. 01). Conclusions Cigarette smoke exposure combined with bacterial infection and 2. 5% adenine induction successfully establishes a model of COPD complicated with CKD in rats, and the inflammatory response might play a major role in the process of COPD complicated with CKD.