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1.
Clin Immunol ; 263: 110232, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38701960

RESUMO

IgA nephropathy (IgAN), which has been confirmed as a complement mediated autoimmune disease, is also one form of glomerulonephritis associated with COVID-19. Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. 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 (33 patients with renal biopsy-proven IgAN experienced COVID-19) compared with Group non-CoV (44 patients with IgAN without COVID-19), respectively. Compared with Group non-CoV, the intensity of glomerular C4d (p = 0.017) and MAC deposition (p < 0.001) and Gd-IgA1 deposition (p = 0.005) were much stronger in Group CoV. Our finding revealed that 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.


Assuntos
COVID-19 , Glomerulonefrite por IGA , SARS-CoV-2 , Humanos , Glomerulonefrite por IGA/imunologia , Glomerulonefrite por IGA/sangue , COVID-19/imunologia , COVID-19/complicações , Feminino , Masculino , Adulto , SARS-CoV-2/imunologia , Pessoa de Meia-Idade , Ativação do Complemento/imunologia , Proteínas do Sistema Complemento/imunologia , Proteínas do Sistema Complemento/metabolismo , Imunoglobulina A/sangue , Imunoglobulina A/imunologia , Glomérulos Renais/patologia , Glomérulos Renais/imunologia , Complemento C5a/imunologia , Complemento C5a/metabolismo
2.
Front Med (Lausanne) ; 9: 945913, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35991640

RESUMO

Introduction: IgA nephropathy (IgAN) encompasses a wide range of clinical and histology features. Some patients present without hematuria, with or without hypertension, still rapidly progress in renal function. Renal pathology of this part of patients were predominant intrarenal arteriolar lesions, rarely presented glomerular proliferative lesions. We aim to investigate the clinical and pathological characteristics and prognosis of these IgAN patients and initially explore whether the abnormal activation of complement is involved in the intrarenal arteriolar lesions of IgAN. Methods: A total of 866 patients with renal biopsy-proven IgAN diagnosed at Beijing Anzhen Hospital were recruited. IgAN patients without intrarenal arteriolar lesions and proliferative lesions were excluded (n = 115), the rest were divided into arteriolar lesions group (n = 202) and proliferative lesions group (n = 549). Among them, 255 patients were regularly followed up for at least 1 year. Renal biopsy tissues of 104 IgAN patients were stained for complement components by immunohistochemistry and immunofluorescence. Results: Compared with proliferative lesions group, the arteriolar lesions group experienced high percentage of hypertension (p = 0.004), low percentage of gross hematuria (p = 0.001), microscopic hematuria (p < 0.001) and less initial proteinuria (p = 0.033). Renal survival between the two groups was not significantly different (p = 0.133). MBL, C4d, FH and FHR5, C3c, and MAC deposited on intrarenal arteriole in arteriolar lesions group. Compare with the proliferative lesion group, the arteriolar lesions group exhibited a higher intensity of C3c deposition on the intrarenal arterioles (p = 0.048). C3c and CD31 co-deposited on intrarenal arterioles area in patients with intrarenal arteriolar lesions. Conclusion: Renal survival of the IgAN patients in arteriolar lesions group was not better than those in proliferative lesions group. Abnormal activation of complement may be involved in the pathogenesis of arteriolar damage through the injury of endothelial cells in this clinical phenotype of IgAN.

3.
Clin Exp Rheumatol ; 28(3): 397-400, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20497632

RESUMO

OBJECTIVES: Although increasing data have supported the possible role of TLR-9 in the pathogenesis of lupus nephritis (LN), the effect of TLR-9 on the lupus phenotype remains controversial. The aim of this study was to associate common variants in the TLR9 gene with susceptibility to lupus nephritis in the Chinese population to further ascertain whether it is a susceptible locus for SLE, especially its likely role in LN from a comparatively large population. METHODS: Two previously reported SLE associated single nucleotide polymorphism (rs352139, rs352140) were investigated in a case-control study comprised of 315 patients with biopsy proven lupus nephritis and 338 matched healthy controls. Single nucleotide polymorphisms (SNPs) were typed by TaqMan allele discrimination assays. RESULTS: Both rs352139 (p=0.040, OR: 0.713, 95%CI: 0.516-0.985) and rs352140 (p=0.048, OR: 0.723, 95%CI: 0.525-0.997) were associated with LN in dominant model. A trend for an association between genotypes and the disease activity indexes was observed. However, no significance was achieved. CONCLUSIONS: The present study suggested that TLR9 gene have a role in establishing an autoimmune background and pathogenesis in human LN.


Assuntos
Povo Asiático/genética , Povo Asiático/estatística & dados numéricos , Nefrite Lúpica/etnologia , Nefrite Lúpica/genética , Polimorfismo de Nucleotídeo Único , Receptor Toll-Like 9/genética , Adulto , China/epidemiologia , Feminino , Predisposição Genética para Doença/etnologia , Haplótipos , Humanos , Desequilíbrio de Ligação , Nefrite Lúpica/imunologia , Masculino , Adulto Jovem
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