الفهرس 
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Abstract
The complement system is an important part of the immune system. It has a critical role in fighting infections and removal of immune complexes and damaged host cells. Uncontrolled overactivation, especially of the self-enhancing alternative pathway, has been implicated in the pathogenesis of different types of glomerulonephritis. Although complement dysregulation is the mainstay of pathogenesis of complement mediated category of glomerulonephritis, a possible auxiliary role in the pathogenesis of immune complex mediated category cannot be excluded.
The aim of the study was to look for genetic variants in two of the most important complement regulating proteins; CFH, as a fluid phase regulator, and MCP, as a tissue surface regulator of complement activity, among some cases of immune complex mediated glomerulonephritis and to correlate the findings with clinical, laboratory, and histopathologic findings in the renal biopsy.
This study included 50 FFPE renal core biopsies, recruited from the archives of pathology department, Alexandria Faculty of Medicine. Twenty-five cases were diagnosed as lupus nephritis and 25 cases were diagnosed as post-infectious glomerulonephritis, as subgroups of the immune complex mediated category of glomerulonephritis. Demographic and clinical data were retrieved from the archived request forms and from the archives of adult and paediatric nephrology units, Alexandria University Hospital. Full histopathologic immunohistochemical study was performed. DNA was extracted from the FFPE tissue. A sequencing library was prepared using Fluidigm Access Array system (Fluidigm Europe B.V, Netherlands). The samples were then sequenced using the Ion 520™ Chip on the Ion S5 XL Semiconductor sequencer (Thermo Fisher, USA).