The complement system is one of the major constituents of the innate immune system that contributes largely to the clearance of foreign substances especially microbes. However, it is has been shown to also damage host tissues in certain pathogenic conditions including various autoimmune diseases.
The kidney is frequently the target of complement activation associated with organ injury. Indeed, low serum complement levels as the result of complement activation are classically known in kidney diseases such as infection-related glomerulonephritis (IRGN), membranoproliferative glomerulonephritis (MPGN), and lupus nephritis. Nowadays, atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy are attracting a lot of attention as the disease due to the aberrant activation of complement alternative pathway. The contribution of complement activation in the disease process has been proved even in the diseases without lowering in serum complement level, such as ANCA-associated vasculitis.
Considering the recent outstanding advance in the field of complement regulating therapy, it would be very important to elucidate the precise complement activation pathway in the disease process. Indeed, various medical agents that control specific point of complement activation, such as C3 (pegcetacopan), C5 (eculizumab), C5aR (avacopan), factor B (iptacopan), factor D (danicopan), and so on, are developing, and are clinically applied to certain pathogenic condition. Therefore, we would like to address the precise mechanism of complement-associated kidney injury, which would unveil the target of therapy for kidney diseases associated with complement activation.
In this Research Topic, we welcome case reports, original research, and review articles in the field, with a focus on but not limited to the kidney injury directly or indirectly related to complement activation, such as AKI, IRGN, C3 glomerulopathy, MPGN, IgA nephropathy, IgA vasculitis, ANCA associated glomerulonephritis, aHUS, acute rejection of transplanted kidney, and thrombotic microangiopathy in the transplanted kidney.
The complement system is one of the major constituents of the innate immune system that contributes largely to the clearance of foreign substances especially microbes. However, it is has been shown to also damage host tissues in certain pathogenic conditions including various autoimmune diseases.
The kidney is frequently the target of complement activation associated with organ injury. Indeed, low serum complement levels as the result of complement activation are classically known in kidney diseases such as infection-related glomerulonephritis (IRGN), membranoproliferative glomerulonephritis (MPGN), and lupus nephritis. Nowadays, atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy are attracting a lot of attention as the disease due to the aberrant activation of complement alternative pathway. The contribution of complement activation in the disease process has been proved even in the diseases without lowering in serum complement level, such as ANCA-associated vasculitis.
Considering the recent outstanding advance in the field of complement regulating therapy, it would be very important to elucidate the precise complement activation pathway in the disease process. Indeed, various medical agents that control specific point of complement activation, such as C3 (pegcetacopan), C5 (eculizumab), C5aR (avacopan), factor B (iptacopan), factor D (danicopan), and so on, are developing, and are clinically applied to certain pathogenic condition. Therefore, we would like to address the precise mechanism of complement-associated kidney injury, which would unveil the target of therapy for kidney diseases associated with complement activation.
In this Research Topic, we welcome case reports, original research, and review articles in the field, with a focus on but not limited to the kidney injury directly or indirectly related to complement activation, such as AKI, IRGN, C3 glomerulopathy, MPGN, IgA nephropathy, IgA vasculitis, ANCA associated glomerulonephritis, aHUS, acute rejection of transplanted kidney, and thrombotic microangiopathy in the transplanted kidney.
