肾病
医学
肠道通透性
内科学
免疫球蛋白A
肾小球肾炎
免疫学
胃肠病学
免疫系统
内分泌学
免疫球蛋白G
肾
糖尿病
作者
Qianqian Li,Xinyi Yuan,Sufang Shi,Lijun Liu,Jicheng Lv,Li Zhu,Hong Zhang
出处
期刊:Ndt Plus
[Oxford University Press]
日期:2022-09-20
卷期号:16 (1): 184-191
被引量:2
摘要
ABSTRACT Background Immunoglobulin A nephropathy (IgAN) and IgA vasculitis with nephritis (IgAV-N) are considered related diseases and share some similar clinicopathologic phenotypes. Elevated circulating galactose-deficient IgA1 (Gd-IgA1)-containing immune complexes and mucosal immunity were associated with the pathogenesis of IgAN and IgAV-N. Recently, studies have identified that the zonulin level, as a modulator of intestinal permeability, is significantly elevated in several inflammatory and autoimmune-related diseases. However, whether zonulin also plays a role in IgAN and IgAV-N is not clear. Methods A total of 73 IgAV-N patients, 68 IgAN patients and 54 healthy controls were assessed for circulating zonulin and Gd-IgA1 levels by enzyme-linked immunosorbent assay. The diagnostic efficiency of the combination of zonulin with Gd-IgA1 was evaluated by the area under the receiver operating characteristic curve (AUC) and integrated discrimination improvement (IDI) analysis. Results Compared with healthy controls, we found that both IgAV-N and IgAN patients had elevated zonulin and Gd-IgA1 levels (P < .001). Additionally, patients with IgAV-N presented with even higher circulating zonulin levels than patients with IgAN (P = .020). The addition of zonulin to Gd-IgA1 showed better predictive performance than Gd-IgA1 alone in the diagnosis of both IgAN and IgAV-N, as illustrated by a significantly increased AUC (IgAN: 0.805 versus 0.708, P = .0021; IgAV-N: 0.886 versus 0.673, P < .001) and significant IDI (IgAN: IDI 0.136, P < .001; IgAV-N: IDI 0.281, P < .001). Conclusion Elevated circulating zonulin levels were detected in both patients with IgAV-N and those with IgAN. Combined detection of circulating zonulin and Gd-IgA1 is recommended as a noninvasive diagnostic biomarker for IgAV-N and IgAN.
科研通智能强力驱动
Strongly Powered by AbleSci AI