Min Chen1, Guang-Qun Xing, Feng Yu, Gang Liu, Ming-Hui Zhao. 1. Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China.
Abstract
BACKGROUND: The pathogenesis of ANCA-associated pauci-immune glomerulonephritis has not been fully elucidated. Several studies had suggested that complement deposition could be detected in renal histopathology. The current study investigated the clinical and pathological significance of complement deposition in renal histopathology of patients with ANCA-associated pauci-immune glomerulonephritis. METHODS: Renal biopsy specimens from 112 patients with ANCA-associated pauci-immune glomerulonephritis were investigated using direct immunofluorescence, light and electron microscopy. For direct immunofluorescence, IgG, IgA, IgM, C3c and C1q staining on fresh frozen renal tissue were routinely performed immediately after a renal biopsy. Complement deposition was defined as the presence of C3c or C1q for at least 1+ in a 0-4+ scale. Clinical and histopathological data between patients with and without complement deposition were compared. RESULTS: In direct immunofluorescence microscopy, C3c and C1q could be detected in glomerular capillary wall and/or mesangium in the specimens of 37/112 (33.0%), 7/112 (6.3%) patients, respectively. Compared with patients without C3c deposition, patients with C3c deposition had a higher level of urinary protein (P < 0.01) and poorer initial renal function (P < 0.05). CONCLUSION: Complement deposition was not rare in renal histopathology of human ANCA-associated pauci-immune glomerulonephritis, which was associated with more severe renal injury.
BACKGROUND: The pathogenesis of ANCA-associated pauci-immune glomerulonephritis has not been fully elucidated. Several studies had suggested that complement deposition could be detected in renal histopathology. The current study investigated the clinical and pathological significance of complement deposition in renal histopathology of patients with ANCA-associated pauci-immune glomerulonephritis. METHODS: Renal biopsy specimens from 112 patients with ANCA-associated pauci-immune glomerulonephritis were investigated using direct immunofluorescence, light and electron microscopy. For direct immunofluorescence, IgG, IgA, IgM, C3c and C1q staining on fresh frozen renal tissue were routinely performed immediately after a renal biopsy. Complement deposition was defined as the presence of C3c or C1q for at least 1+ in a 0-4+ scale. Clinical and histopathological data between patients with and without complement deposition were compared. RESULTS: In direct immunofluorescence microscopy, C3c and C1q could be detected in glomerular capillary wall and/or mesangium in the specimens of 37/112 (33.0%), 7/112 (6.3%) patients, respectively. Compared with patients without C3c deposition, patients with C3c deposition had a higher level of urinary protein (P < 0.01) and poorer initial renal function (P < 0.05). CONCLUSION: Complement deposition was not rare in renal histopathology of human ANCA-associated pauci-immune glomerulonephritis, which was associated with more severe renal injury.