| 초록 |
Objectives: Since the coronavirus disease of 2019 (COVID-19) pandemic swept across the world, the flare of immune-mediated disease following SARS-CoV-2 infection has emerged rapidly. IgA nephropathy (IgAN), which has been confirmed as a complement mediated autoimmune disease, is also one of the common glomerulonephritis associated with COVID-19. Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. Methods: 33 patients with renal biopsy-proven IgAN (Group CoV) who had experienced COVID-19 before renal biopsy were enrolled. Meanwhile, 44 patients with IgAN (Group non-CoV) without COVID-19 were enrolled as control. Complement proteins and Gd-IgA1 were detected by enzyme-linked immunosorbent assay and immunofluorescence. SARS-CoV-2 nucleocapsidin was detected by immunohistochemistry. Clinicopathological and immunological features between the two groups were analyzed. Results: Compared with Group non-CoV, the level of eGFR was significantly lower in Group CoV (p=0.010). Histologically, compared with Group non-CoV, Group CoV presented with more percentages of segmental glomerulosclerosis/adhesion (p=0.003) and less percentages of mesangial hypercellularity (p=0.017). The level of plasma level of C5a (p<0.001), soluble C5b-9 (p=0.018), FHR5 (p<0.001) were all significantly higher in Group CoV compared with Group non-CoV, respectively. Compared with Group non-CoV, the intensity of glomerular MAC deposition was much stronger in Group CoV (p=0.246). There were no significantly different in serum levels of IgA, Gd-IgA1, IgA immune complex between two Groups. However, a greater intensity of Gd-IgA1 deposition in glomerular mesangial and capillary areas has been exhibited in Group CoV than those in Group non-CoV (p=0.005). Conclusions: For IgAN after COVID-19, mucosal immune responses to SARS-CoV-2 infection may result in the overactivation of systemic and renal local complement system, and increased glomerular deposition of Gd-IgA1, which may lead to renal dysfunction and promote renal progression in IgAN patients. |