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[Changes in the complement system in membranoproliferative glomerulonephritis].
AIM: To compare the clinical manifestations membranoproliferative glomerulonephritis (MPGN) in its idiopathic variant, lupus nephritis (LN), and C3 glomerulopathy (C3-GP), by comparing them with changes in the complement system.
SUBJECTS AND METHODS: The clinic of nephrology followed up 42 patients with different types of MPGN in 2013 to 2015. The study included 35 patients divided into 3 groups: 1) 8 patients with C3-GP, 2) 13 with idiopathic MPGN; 3) 14 with Class IV LN. The investigators studied the blood and urine levels of components and markers for activation of the classical and alternative pathways (C3 and C4, С3а, C5a, CFH, CFB, and CFD) of the terminal complement complex (TCC).
RESULTS: The detection rate of C3-GP was 19%. The patients with C3-GP were noted to have the lowest blood concentration of S3 and the highest urinary level of С3а, C5a, TCC, CFH, CFB, and CFD. C3 nephritic factor was detected in 2 patients from the C3-GP (dense deposit disease) group.
CONCLUSION: Alternative complement pathway dysregulation caused by genetic or autoimmune factors plays a leading role in the pathogenesis of C3-GP.
SUBJECTS AND METHODS: The clinic of nephrology followed up 42 patients with different types of MPGN in 2013 to 2015. The study included 35 patients divided into 3 groups: 1) 8 patients with C3-GP, 2) 13 with idiopathic MPGN; 3) 14 with Class IV LN. The investigators studied the blood and urine levels of components and markers for activation of the classical and alternative pathways (C3 and C4, С3а, C5a, CFH, CFB, and CFD) of the terminal complement complex (TCC).
RESULTS: The detection rate of C3-GP was 19%. The patients with C3-GP were noted to have the lowest blood concentration of S3 and the highest urinary level of С3а, C5a, TCC, CFH, CFB, and CFD. C3 nephritic factor was detected in 2 patients from the C3-GP (dense deposit disease) group.
CONCLUSION: Alternative complement pathway dysregulation caused by genetic or autoimmune factors plays a leading role in the pathogenesis of C3-GP.
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