Fig 1.
Glomerular staining intensity of IgA and galactose-deficient IgA1.
Double staining with anti-IgA polyclonal antibody and Gd-IgA1 (KM55) monoclonal antibody was performed on biopsy specimens. Representative images of glomerular IgA and Gd-IgA1 (KM55) in patients with 0, 1+, 2+, and 3+ staining intensity. Seventy-four patients were divided into four groups according to the staining intensity of IgA: group 0 (n = 4), group 1+ (n = 46), group 2+ (n = 12), and group 3+ (n = 12). These patients were also divided into four groups according to the staining intensity of Gd-IgA1: group 0 (n = 4), group 1+ (n = 35), group 2+ (n = 23), and group 3+ (n = 12). Fluorescein-conjugated polyclonal rabbit anti-human IgA antibody (DAKO Japan Inc., Kyoto, Japan), anti-human Gd-IgA1 antibody (KM55) (Immuno-Biological Laboratories Co., Ltd, Gunma, Japan), and Alexa Fluor 555-conjugated goat anti-rat IgG antibody (Life Technologies) was used for immunofluorescence staining. Original magnification: ×200. Gd-IgA1, galactose-deficient IgA1.
Fig 2.
Association between glomerular staining intensity of IgA and galactose-deficient IgA1 (Gd-IgA1) and the rate of cnm-positive S. mutans in the oral cavity.
Comparison of the glomerular staining intensity of IgA and the positive rate of S. mutans in the oral cavity (a). Comparison of the glomerular staining intensity of IgA and the positive rate of cnm-positive S. mutans in the oral cavity (b). Comparison of the glomerular staining intensity of Gd-IgA1 (KM55) and the positive rate of S. mutans in the oral cavity (c). Comparison of the glomerular staining intensity of Gd-IgA1 (KM55) and the positive rate of cnm-positive S. mutans in the oral cavity (d). Data were analyzed using the Cochran–Armitage trend test. P < 0.05 was considered statistically significant.
Table 1.
Comparison between the cnm-positive and cnm-negative S. mutans groups of patients.
Table 2.
Analysis of renal biopsy specimens using the Oxford classification.