Abstract: Ｏｂｊｅｃｔｉｖｅ：The article was based on urinary proteomics to screen for differentially expressed proteins in IgAN. It may explore the pathogenesis of IgAN and provide new clues for the discovery of potential biomarkers.
Ｍｅｔｈｏｄｏｌｏｇｙ：Urine proteomic data from patients with IgAN and membranous nephropathy, as well as healthy individuals, were analyzed. Patients with membranous nephropathy and healthy individuals were used as controls to screen for differentially expressed proteins in IgAN. The protein Plexin-B2 was to be analyzed for correlation with clinicopathological indicators. The expression of Plexin-B2 and its ligand angiogenin (ANG) in blood and urine was detected and verified by enzyme-linked immunosorbent assay (ELISA) and their expression in renal tissues was detected by immunohistochemistry.
Ｒｅｓｕｌｔｓ：Urinary Plexin-B2 (uPlexin-B2) expression was significantly increased in IgAN patients as detected by mass spectrometry compared to healthy controls. And it was positively correlated with total cholesterol (r=0.34, P=0.02) and LDL (r=0.43, P=0.01). Urinary Plexin-B2 was negatively correlated with segmental glomerulosclerosis (r=-0.28, P=0.04). A trend of elevated uPlexin-B2 in IgAN patients was found by ELISA. The expression level of ANG was significantly higher in the blood of IgAN patients than in the healthy group (61.97 vs. 6.30, P<0.001). ANG in the blood was negatively correlated with endocapillary hypercellularity (r=-0.40, P=0.04) and with the number of segmental sclerosis (r=-0.44, P=0.04). uPlexin-B2 was negatively correlated with the number of glomerulosclerosis (r=-0.95, P=0.01). Both Plexin-B2 and ANG were highly expressed in renal tubules in IgAN.
Ｃｏｎｃｌｕｓｉｏｎ：Urinary Plexin-B2 was increased in patients with IgAN. Plexin-B2 and ANG were significantly associated with glomerulosclerosis in IgAN. Moreover, ANG was notably elevated in the blood of patients with IgAN. The article could provide clues for the discovery of potential biomarkers and provide new insight into the pathogenesis of renal pathology in IgAN.