Tonsillitis exacerbates renal injury in IgA nephropathy through promoting Th22 cells chemotaxis

2018 ◽  
Vol 50 (7) ◽  
pp. 1285-1292 ◽  
Author(s):  
Lu Gan ◽  
Mengyuan Zhu ◽  
Xiaozhao Li ◽  
Chen Chen ◽  
Ting Meng ◽  
...  
2014 ◽  
Vol 306 (8) ◽  
pp. F885-F895 ◽  
Author(s):  
Qiongzhen Lin ◽  
Ying Chen ◽  
Jicheng Lv ◽  
Hong Zhang ◽  
Jiawei Tang ◽  
...  

Tubulointerstitial injury plays an important role in the development and progression of chronic kidney disease (CKD). Kidney injury molecule (KIM)-1 is induced in damaged proximal tubules in both acute renal injury and CKD. However, the dynamics of KIM-1 in CKD and effects of KIM-1 expression on disease progression are unknown. Here, we aimed to determine the associations between tubular KIM-1 expression levels, renal function, and inflammation in CKD. The relationships between levels of KIM-1 and clinicopathological parameters were analyzed in patients with progressive and nonprogressive IgA nephropathy. KIM-1 expression was increased in patients with IgA nephropathy, and its expression was significantly correlated with the decrease of renal function. KIM-1 was particularly evident at the site with reduced capillary density, and KIM-1-positive tubules were surrounded by infiltrates of inflammatory cells. Using in vitro cell models, we showed that cellular stressors, including hypoxia, induced KIM-1 expression. KIM-1-expressing cells produced more chemokines/cytokines when cultured under hypoxic conditions. Furthermore, we showed that tubular cells with KIM-1 expression can regulate the immune response of inflammatory cells through the secretion of chemotactic factors. These data suggest that KIM-1-expressing epithelial cells may play a role in the pathogenesis of tubulointerstitial inflammation during chronic renal injury through the secretion of chemokines/cytokines.


2003 ◽  
Vol 23 (3) ◽  
pp. 121-128 ◽  
Author(s):  
Pilar Arrizabalaga ◽  
Manel Solé ◽  
Rosa Abellana ◽  
Xavier de las Cuevas ◽  
Josep Soler ◽  
...  
Keyword(s):  

2013 ◽  
Vol 74 (12) ◽  
pp. 1586-1591 ◽  
Author(s):  
Zhiguo Peng ◽  
Jun Tian ◽  
Xianquan Cui ◽  
Wanhua Xian ◽  
Huaibin Sun ◽  
...  

1999 ◽  
Vol 10 (1) ◽  
pp. 101-109
Author(s):  
NORISHIGE YOSHIKAWA ◽  
HIROSHI ITO ◽  
TADASU SAKAI ◽  
YASUO TAKEKOSHI ◽  
MASATAKA HONDA ◽  
...  

Abstract. The most appropriate treatment for patients with IgA nephropathy is controversial. Treatment with prednisolone, azathioprine, heparin-warfarin, and dipyridamole early in the course of disease may prevent immunologic renal injury in children with severe IgA nephropathy. To determine whether similar results can be obtained with a combination of just heparin-warfarin and dipyridamole, the effects of such treatment were compared to those of treatment with prednisolone, azathioprine, heparin-warfarin, and dipyridamole in 78 children with newly diagnosed IgA nephropathy showing diffuse mesangial proliferation. The patients were randomly assigned to receive either prednisolone, azathioprine, heparin-warfarin, and dipyridamole for 2 yr (group 1) or heparin-warfarin and dipyridamole for 2 yr (group 2). All of the 40 patients in group 1 and 34 of the 38 patients in group 2 completed the trial. The mean urinary protein excretion fell in group 1 patients (P < 0.0001), but remained unchanged in group 2 patients. The mean serum IgA concentration was reduced in group 1 patients (P = 0.0002), but was unchanged in group 2 patients. BP and creatinine clearance were normal at the end of the trial in all but one group 2 patient, who developed chronic renal insufficiency. The percentage of glomeruli showing sclerosis was unchanged in group 1 patients, but increased in group 2 patients (P = 0.006). The intensity of mesangial IgA deposits decreased in group 1 patients (P = 0.02), but remained unchanged in group 2 patients. In conclusion, the present study shows that treatment of children with severe IgA nephropathy with prednisolone, azathioprine, heparin-warfarin, and dipyridamole for 2 yr early in the course of disease reduces immunologic renal injury and prevents increase of sclerosed glomeruli.


2017 ◽  
Vol 441 (1-2) ◽  
pp. 191-199 ◽  
Author(s):  
Lu Gan ◽  
Qiaoling Zhou ◽  
Xiaozhao Li ◽  
Chen Chen ◽  
Ting Meng ◽  
...  

2020 ◽  
Vol 87 ◽  
pp. 106789
Author(s):  
Yong Zhong ◽  
Rong Tang ◽  
Yang Lu ◽  
Wei Wang ◽  
Chenggen xiao ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Ke Su ◽  
Ping Zeng ◽  
Wei Liang ◽  
Zhengyu Luo ◽  
Yiman Wang ◽  
...  

FTY720, a new chemical substance derived from the ascomyceteIsaria sinclairii, is used for treating multiple sclerosis, renal cancer, and asthma. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid metabolite and exists in red blood cells. FTY720 is a synthetic S1P analog which can block S1P evoking physiological effects. Recently studies show that S1P was participating in activated inflammation cells induced renal injury. The objective of this study was to assess the protective effect of FTY720 on kidney damage and the potential mechanism of FTY720 which alleviate podocyte injury in chronic kidney disease. In this study, we selected 40 patients with IgA nephropathy and examined their clinical characteristics. Ang II-infusion rat renal injury model was established to evaluate the glomeruli and tubulointerstitial lesion. The result showed that the concentration of S1P in serum and urine was positively correlated with IgA nephropathy patients’ renal injury. FTY720 could reduce renal histological lesions induced by Ang II-infusion in rats. Moreover, FTY720 decreased S1P synthesis in Ang II-infusion rats via downregulation of inflammatory cytokines including TNF-αand IL-6. In addition, FTY720 alleviated exogenous S1P-induced podocyte damage. In conclusion, FTY720 is able to attenuate S1P-induced podocyte damage via reducing inflammatory cytokines.


2017 ◽  
Vol 42 ◽  
pp. 203-208 ◽  
Author(s):  
Chenggen Xiao ◽  
Qiaoling Zhou ◽  
Xiaozhao Li ◽  
Hui Li ◽  
Yong Zhong ◽  
...  
Keyword(s):  

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