Correlation between the mechanism of arteriopathy in IgA nephropathy and blood stasis syndrome: A cohort study.

To investigate the correlation between blood stasis syndrome and arteriopathy in immunoglobulin A nephropathy (IgAN). Wall thickness/outer vessel diameter, intimal thickness/outer vessel diameter, and medial thickness/outer vessel diameter were measured using ImageJ software. Vascular endothelial-derived growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), proliferating cell nuclear antigen (PCNA), extracellular signal-regulated kinase (ERK) 1/2, and nuclear factor kappa B (NF-κB) were detected by immunohistochemical staining. Twenty-four-hour urine protein quantification, serum creatinine, urea nitrogen, and uric acid were collected. Blood stasis syndrome and vessel scores were calculated based on Katafuchi's grade. Intimal thickness/outer vessel diameter (0.2725 ± 0.0932 μm), medial thickness/outer vessel diameter (0.2747 ± 0.1139 μm), and wall thickness/outer vessel diameter (0.6136 ± 0.1120 μm) were the largest in IgAN with arteriopathy group. VEGF (0.35 ± 0.90), MMP-9 (0.38 ± 0.12), PCNA (0.43 ± 0.12), ERK1/2 (0.31 ± 0.11), and NF-κB (0.37 ± 0.14) were the highest in IgAN with arteriopathy group. Intimal thickening of IgAN was moderately positively correlated with VEGF, MMP-9, PCNA, ERK1/2, and NF-κB (0.5 < r < 0.8). Medial thickening of IgAN was moderately positively correlated with PCNA and NF-κB (0.5 < r < 0.8). Wall thickening of IgAN was lowly positively correlated with VEGF and MMP-9 (0.3 < r < 0.5). Blood stasis syndrome score was associated with vessel score in IgAN with arteriopathy (P < 0.05). Blood stasis syndrome score can assess the degree of pathological changes.