MO549: Chronic Kidney Disease and Vascular Calcification Result in Inflammation and Dysfunction of Colon Tissue in Rats

Abstract

Abstract BACKGROUND AND AIMS Chronic Kidney Disease (CKD) results in modifications in the activity and/or structure of many organs. One of them is the intestine. Intestinal barrier dysfunction may result in turn, in gut leakage and aggravation of the course of CKD. The interaction between the colon and kidneys may be relevant for both, the kidneys as well as the colon. This study aimed to evaluate the impact of CKD and vascular calcification on colon tissue and function. METHOD Sprague–Dawley rats underwent 5/6 nephrectomy (SNx, n = 18) or sham surgery (Control, n = 6). A total of 8 weeks after surgery, SNx rats were divided into three groups: normal chow (SNx, n = 6); high phosphate (1.2%) with high vitamin D; 5 days/week at a dose of 0.1 µg/day (SNx-VC1, n = 6) or 0.4 µg/day (SNx-VC2, n = 6) to induce vascular calcification. Four weeks after dietary intervention, rats were sacrificed and colon tissue was sampled for analysis. The inflammation of colon tissue was scored on haematoxylin-eosin staining (score 1–4) and the presence of macrophages was quantified by immunostaining with CD68 antibody. The mucus production was also quantified by Alcian blue staining. RESULTS Haematoxylin-eosin staining showed increased inflammation in SNx-VC2 rats (2.47 ± 0.26) compared with the Control group (1.52 ± 0.14) (P < 0.05), Figure 1. The number of CD68 + cells did not differ between groups. Compared with the Control group (19.87 ± 2.20), mucus production was reduced significantly in SNx-VC2 rats (11.98 ± 2.61) (P < 0.05) and close to significance (P < 0.0505) in SNx-VC1 (13.21 ± 1.22). CONCLUSION CKD was associated with a decrease in mucus production and an increase in inflammation in colon tissue. These changes are more marked in the animals with associated vascular calcification (high vitamin D and high phosphate diet).