Deciphering the Genetic Code of Autoimmune Kidney Diseases

Autoimmune kidney diseases occur due to the loss of tolerance to self-antigens, resulting in inflammation and pathological damage to the kidneys. This review focuses on the known genetic associations of the major autoimmune kidney diseases that result in the development of glomerulonephritis: lupus nephritis (LN), anti-neutrophil cytoplasmic associated vasculitis (AAV), anti-glomerular basement disease (also known as Goodpasture's disease), IgA nephropathy (IgAN), and membranous nephritis (MN). Genetic associations with an increased risk of disease are not only associated with polymorphisms in the human leukocyte antigen (HLA) II region, which governs underlying processes in the development of autoimmunity, but are also associated with genes regulating inflammation, such as NFkB, IRF4, and FC ? receptors (FCGR). Critical genome-wide association studies are discussed both to reveal similarities in gene polymorphisms between autoimmune kidney diseases and to explicate differential risks in different ethnicities. Lastly, we review the role of neutrophil extracellular traps, critical inducers of inflammation in LN, AAV, and anti-GBM disease, where inefficient clearance due to polymorphisms in DNase I and genes that regulate neutrophil extracellular trap production are associated with autoimmune kidney diseases.

Automated summary

Autoimmune kidney diseases occur due to the loss of self-antigen tolerance, leading to inflammation and pathological damage to the kidneys. This review focuses on the genetic associations of major autoimmune kidney diseases, including lupus nephritis, anti-neutrophil cytoplasmic associated vasculitis, anti-glomerular basement disease, IgA nephropathy, and membranous nephritis. Genetic associations are not only linked to polymorphisms in the human leukocyte antigen II region, but also to genes regulating inflammation. The article also discusses genome-wide association studies to uncover similarities and differences in gene polymorphisms among different ethnicities. Finally, the role of neutrophil extracellular traps in inflammation and autoimmune kidney diseases is reviewed.