Objective To investigate secretory IgA change in uremic patients ane its relationship with inflammation. Methods Sixty uremic noneialysis patients( uremic non eialysis group)ane 60 hemoeialysis patients( hemoeialysis group ),the other 40 healthy volunteers( control group ) were selectee as our subjects. Enzyme linkee immunosorbent assay( ELISA)methoe were appliee to eetect the fecal secretory IgA content. Immune nephelometry were usee to measure the level of high sensitivity C reactive protein(hs-CRP). Results The level of fecal secretory IgA expression in hemoeialysis group((2. 39 ± 0. 81)μmol/ L)ane the non eialysis group((2. 43 ± 0. 84)μmol/ L)were significantly lower than that of the control group((2. 89 ± 0. 87)μmol/ L),ane the eifference was significant(F = 5. 042,P < 0. 01),while there was no significant eifference between the eialysis group ane the non eialysis group(P > 0. 05). The negative correlation was seen between secretory IgA content ane hs-CRP in patients(r = - 0. 629,P < 0. 01). Conclusion The secretory IgA eecreasee in patients with or without uremic eialysis ane it is correlatee with inflammatory state.

Objective:To explore the construction of abdominal aortocaval fistula (ACF) model in adenine-induced renal failure rats, and to provide a suitable animal model for subsequent mechanism and intervention researches.Methods:Adult female Sprague-Dawley rats (250-300 g) were fed with 0.75% adenine diet (renal failure group, n=60) and the same diet without adenine (control group, n=10) for 4 weeks, and the rats were randomly grouped by block randomization method with a ratio of 6∶1. Thirty rats in the renal failure group were randomly selected by block randomization method at a ratio of 1∶1 to undergo laparotomies to establish ACF models (renal failure+ACF group). The serum creatinine, blood urea nitrogen detection and Masson staining were used to evaluate the establishment of renal failure model. Small animal ultrasound imaging system was applied to verify the successful construction of the ACF model. After 6 weeks of ACF observation, blood samples were collected from the heart of rats, and ACF-vascular tissues were collected for pathological study (HE staining). Results:At 4 weeks of feeding, compared with the control group, serum creatinine [(63.8±23.5) μmol/L vs. (33.0±3.8) μmol/L, Z=3.651, P<0.001] and blood urea nitrogen [(13.1±6.9) mmol/L vs. (5.3±0.6) mmol/L, Z=3.254, P=0.001] in the renal failure group were both higher. Masson staining showed renal tubulointerstitial inflammatory cell infiltration, renal tubular epithelial cell atrophy, interstitial fibrosis and vascular injury. Five rats sacrificed after ACF surgeries, and the survival rate was 83.3%. Doppler ultrasound showed turbulent blood flow of arterial to venous shunt at the anastomosis of open ACF (23/25) in the renal failure+ACF group. HE staining showed typical eccentric neointimal hyperplasia in the outflow tract of ACF vein in the renal failure+ACF group. Conclusions:The adenine-induced ACF rat model is successfully constructed, and ACF shows typical eccentric neointimal hyperplasia. The ACF construction would provide a reliable animal model to study the mechanism and intervention of neointimal hyperplasia for autologous arteriovenous fistula.