About this Research Topic
Immune-mediated kidney injury is one of the major causes of nephrotic syndrome and chronic kidney disease worldwide, often leading to end-stage kidney disease requiring dialysis and kidney graft. Immune-mediated kidney diseases are characterised by circulating autoantibodies that may cause organ-restricted damage, such as in IgA nephropathy, membranous nephropathy, membranoproliferative glomerulonephritis, anti-glomerular basement membrane glomerulonephritis, and C3 glomerulopathy. In these pathologies autoantibodies may be deposited at the glomerular basement membrane alongside target autoantigens and complement proteins causing podocyte damage and leading to proteinuria. Immune-mediated injury may also arise as a consequence of a systemic disorder, such as in lupus erythematosus (SLE) or anti-neutrophil cytoplasmic antibody (ANCA) vasculitis. The course of disease is highly variable even within the same pathology.
Significant progress has been made in the last decade elucidating the pathophysiological mechanisms of these diseases, including the discovery of several new target autoantigens in membranous nephropathy, as well as the establishment of animal models. However, the causes and triggers for many autoimmune nephropathies are not well understood. Accordingly, treatment options remain limited in the absence of target-specific treatment which is most often replaced by the use of wide-range immunosuppressive drugs. While immunosuppressors have shown remarkable results in clinical trials for diseases such as membranous nephropathy, challenges remain in identifying the best course of action depending on the clinical status and severity of the disease with the goal of improving efficacy and limiting toxic side-effects.
This special collection accepts articles related to all nephropathies mediated by autoantibodies. We welcome manuscripts focusing on, but not limited to, the following topics of interest:
- The prevalence and prognostic value of newly identified and already established biomarkers: from target autoantigens to immune biomarkers
- Pathophysiological mechanisms of antibodies-mediated nephropathies: from bench to bedside and back to bench
- The role of genes and environment in the pathogenesis of autoantibodies-mediated nephropathies
- New therapeutic targets and (re)evaluation of existing treatment options
- New tools for more efficient monitoring of patients’ clinical and immunological status
Significant progress has been made in the last decade elucidating the pathophysiological mechanisms of these diseases, including the discovery of several new target autoantigens in membranous nephropathy, as well as the establishment of animal models. However, the causes and triggers for many autoimmune nephropathies are not well understood. Accordingly, treatment options remain limited in the absence of target-specific treatment which is most often replaced by the use of wide-range immunosuppressive drugs. While immunosuppressors have shown remarkable results in clinical trials for diseases such as membranous nephropathy, challenges remain in identifying the best course of action depending on the clinical status and severity of the disease with the goal of improving efficacy and limiting toxic side-effects.
This special collection accepts articles related to all nephropathies mediated by autoantibodies. We welcome manuscripts focusing on, but not limited to, the following topics of interest:
- The prevalence and prognostic value of newly identified and already established biomarkers: from target autoantigens to immune biomarkers
- Pathophysiological mechanisms of antibodies-mediated nephropathies: from bench to bedside and back to bench
- The role of genes and environment in the pathogenesis of autoantibodies-mediated nephropathies
- New therapeutic targets and (re)evaluation of existing treatment options
- New tools for more efficient monitoring of patients’ clinical and immunological status
Keywords: nephropathy, glomerulonephritis, immunosuppressive treatment, biomarker, autoantibodies, podocyte
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