Clinical nephrology · 2021
Association between anti-complement factor H antibodies and renal outcome in primary membranous nephropathy.
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Kagaya Yu, Hayashi Norifumi, Fujimoto Keiji, Adachi Hiroki, Furuichi Kengo, Yokoyama Hitoshi
Аннотация
AIMS: The complement factor H (CFH) is a regulator for the alternative complement pathway. The prevalence and roles of anti-CFH antibodies in the clinical outcome of primary membranous nephropathy (MN) patients remain unclear.
MATERIALS AND METHODS: A total of 106 biopsy-proven kidney disease patients and 18 healthy controls were retrospectively investigated in this study. 36 patients had primary MN and 70 patients were diseased controls (31 minimal change nephrotic syndrome (MCNS), 19 rapidly progressive glomerulonephritis (RPGN), and 20 IgA glomerulonephritis (IgAGN)). Serum anti-CFH antibody titers were measured by enzyme-linked immunosorbent assay.
RESULTS: 77.8% of MN patients were positive for anti-CFH antibodies. However, only 27.1% of diseased control patients and 5.6% of healthy controls were positive for anti-CFH antibodies. Moreover, median anti-CFH antibody titers were significantly higher in MN patients (4.69 AU/mL) than in diseased control patients (MCNS patients (0 AU/mL, p < 0.01), RPGN patients (0 AU/mL, p < 0.05), IgAGN patients (0 AU/mL, p < 0.01)), and healthy controls (0 AU/mL, p < 0.01). Anti-CFH antibody titer was selected as an independent unfavorable predictor of renal dysfunction by Cox proportional hazards analysis.
CONCLUSION: These data suggest that anti-CFH antibodies may be involved in the deterioration of renal function in primary MN.
MATERIALS AND METHODS: A total of 106 biopsy-proven kidney disease patients and 18 healthy controls were retrospectively investigated in this study. 36 patients had primary MN and 70 patients were diseased controls (31 minimal change nephrotic syndrome (MCNS), 19 rapidly progressive glomerulonephritis (RPGN), and 20 IgA glomerulonephritis (IgAGN)). Serum anti-CFH antibody titers were measured by enzyme-linked immunosorbent assay.
RESULTS: 77.8% of MN patients were positive for anti-CFH antibodies. However, only 27.1% of diseased control patients and 5.6% of healthy controls were positive for anti-CFH antibodies. Moreover, median anti-CFH antibody titers were significantly higher in MN patients (4.69 AU/mL) than in diseased control patients (MCNS patients (0 AU/mL, p < 0.01), RPGN patients (0 AU/mL, p < 0.05), IgAGN patients (0 AU/mL, p < 0.01)), and healthy controls (0 AU/mL, p < 0.01). Anti-CFH antibody titer was selected as an independent unfavorable predictor of renal dysfunction by Cox proportional hazards analysis.
CONCLUSION: These data suggest that anti-CFH antibodies may be involved in the deterioration of renal function in primary MN.