Table 1.
Baseline characteristics and therapeutic regimens of 111 patients with IgAN.
Table 2.
Comparison of characteristics among patients with IgAN and other kidney diseases.
Fig 1.
Serum-Gd-IgA1 levels determined by ELISA using KM55.
Serum-Gd-IgA1 in patients with IgAN, HPN, LN, AAV, and MCD (A). S-Gd-IgA1 in patients with IgAN according to JSN classification in terms of clinical grade (B), histological grade (C), and risk classification of progression to ESKD (D). Horizontal solid lines represent means. Data were statistically analyzed using Kruskal-Wallis tests and Mann-Whitney U tests.
Fig 2.
Glomerular m-Gd-IgA1 deposition identified by IHC staining for KM55.
Representative photos of glomerular m-Gd-IgA1 (brown reaction product) in patients with MCD (A), LN (B), HSPN (C), and IgAN (D-F). Original magnification: ×40. Intensity of glomerular m-Gd-IgA1 compared between IgAN and other kidney diseases (G). Intensity of m-Gd-IgA1 in IgAN according to JSN histological grade (H). Correlation between m-Gd-IgA1 positivity and s-Gd-IgA1 level in patients with IgAN (I). Horizontal solid lines represent means. Data were statistically analyzed using Kruskal-Wallis tests, Mann-Whitney U tests, and Spearman correlations.
Fig 3.
Correlations between s-Gd-IgA1 and laboratory parameters or pathological findings in patients with IgAN.
Scatter plots of s-Gd-IgA1 vs. serum IgA (A), serum IgA/C3 ratio (B), proteinuria (C), sCr (D), eGFR (E), urinary NAG index (F), global sclerosis (G), crescents (H), and global sclerosis and crescents (I). Rates of global sclerosis, crescents, and both types of glomerular lesions (%) were calculated by dividing total number of each type of lesion by total number of glomeruli. Crescents comprise cellular, fibrocellular, and fibrous types. S-Gd-IgA1 levels were compared based on Oxford classification (J-M). Patients with IgAN were assigned to groups according to mesangial hypercellularity (J), endocapillary hypercellularity (K), segmental glomerulosclerosis (L) and tubular atrophy/interstitial fibrosis (M). Horizontal solid lines represent means. Data were statistically analyzed using Mann-Whitney U tests and Spearman correlation tests.
Fig 4.
Correlations between m-Gd-IgA1 deposition and laboratory parameters or pathological findings in patients with IgAN.
Scatter plots of m-Gd-IgA1 intensity vs. serum IgA (A), serum IgA/C3 ratio (B), proteinuria (C), sCr (D), eGFR (E), urinary NAG index (F), global sclerosis (G), crescents (H), and global sclerosis and crescents (I). Rates of global sclerosis, crescents, and both glomerular lesions (%) were calculated by dividing total numbers of each lesion by otal number of glomeruli. Crescents comprised cellular, fibrocellular, and fibrous types. Mesangial-Gd-IgA1 intensity was compared based on Oxford classification (J-M). Patients with IgAN were assigned to groups according to mesangial hypercellularity (J), endocapillary hypercellularity (K), segmental glomerulosclerosis (L), and tubular atrophy/interstitial fibrosis (M). Horizontal solid lines represent means. Data were statistically analyzed using Mann-Whitney U tests and Spearman correlation tests.
Table 3.
Univariate and multivariate analysis of possible factors that contributed to 30% eGFR reduction in 111 patients with IgAN.