Objective To study the expression characteristics of intestinal exosomes carrying miR-146a in rats with chronic kidney disease (CKD) micro-inflammation. Methods Sixteen healthy SPF-grade Wistar male rats were randomly divided into two groups: the normol group and the model group. An adenine-induced CKD rat model was used. After 3 days of adaptive feeding, rats were gavaged with a gastric adenine shock dose of 220 mg/ (kg·d) for 4 weeks and a maintenance dose of 100 mg/ kg for 3 weeks for a total of 7 weeks. At the end of the experiment, after anesthesia, blood was taken from the mid-abdominal artery of the rats. Serum and anticoagulant plasma with EDTA are left behind. For the determination of blood urea nitrogen (BUN) and creatinine (Cr) in serum, By enzyme-linked immunosorbent assay (ELISA), we determined levels of serum interleukin-1, interleukin-6 and tumor necrosis factor. Histopathological observation of kidney sections was performed, including an examination of kidney histomorphology by hematoxylin and eosin staining and kidney fibrosis by Masson staining. Transmission electron microscopy was used to observe the intestinal tissue ultrastructure and exosome secretion. Plasma exosomes were extracted from intestinal tissues via a reagent kit method and ultra-high speed centrifugation. Negative-stain electron microscopy was used in the identification of exosome morphology, and the NTA technique was used to determine exosome particle size. Western blot assays were employed to examine exosome surface biomarkers. Reverse transcription-polymerase chain reaction was used to detect the expression level of miR-146a in plasma exosomes. Western blot was used to determine the presence of tumor necrosis factor receptor-associated factor 6 (TRAF6), nuclear factor-κB (NF-κB), and Toll-like receptor 4 (TLR4) inflammatory signaling pathway proteins in the intestinal tissues. Results A CKD rat model was formed after 7 weeks of adenine gavage, and the model was characterized by a significant increase in serum BUN and Cr levels compared with the control group (P<0. 01). Serum and ileal tissue levels of IL-1β, IL-6, and TNF-α were significantly higher in the model group than the control group (P<0. 01). Pathology of the model group revealed atrophied and expanded renal tubules, cystic lesions, and many brown crystals found in the renal cortex glomerulosclerosis, glomerular atrophy, Bowman’s cystic cavity dilatation. Clearly there is a reduction in the number of Bowman’s capsules and a difference in the size of the capsule cavity. The model grouped showed obvious interstitial fibrosis and inflammatory cell infiltration. Exosomes of 155 nm were found in the plasma and intestinal tissues of rats in the model group, and transmission electron microscopy revealed that a large number of exosomes were released from the intestinal tissues. The number of plasma exosomes carrying miR-146a in the model group was significantly higher than that in the control group (P<0. 01), whereas the number of intestinal exosomes carrying miR-146a was significantly lower than that in the control group (P<0. 01). Conclusions Adenine causes chronic renal failure with impaired kidney function and morphological pathological changes with systemic microinflammation in rats. Exosomes are secreted and released from the intestinal tissues of CKD rats, Resulting in the increased activation of plasma exosomes carrying miR-146a.