Inflammation, immunity, and autoimmunity in glomerulopathy: pre- and post-transplant

To comprehensively address the various pathways that can lead to GN/NS so that individualized mechanisms and cellular targets can be identified. This may lead to personalized therapy so that broad-spectrum therapy with high-dose steroids, and Plasmapheresis (PP) may no longer be necessary.Glomerulonephritis (GN) is a significant cause of nephrotic syndrome (NS) and Chronic Kidney Disease (CKD). Although the Podocyte (Podo) is felt to be the most significant target in the development of GN/NS, other cells and mechanisms are being recently described that may contribute to Podo injury or be the primary target. These cells include endothelial cells, macrophages, lymphocytes (B and T cells), mesangial cells, etc. The mechanisms may include circulating factors, generally known as danger signals, but perhaps more specifically,anti-Nephrin antibodies in recently described autoimmune anti-Podocyte GN.1) Involvement of Endothelial Cells (EC) 2) Autoimmunity/anti-Nephrin autoantibodies 3) Involvement of sphingolipids 4) Effects of the Microbiome 5) cGAS-STING mechanisms in renal injury 6) Innate and Adaptive Immune activity in GN/NS 7) Biomarkers identified in GN/NS 8) Role of Circulating Factors in GN/NS 9) Inflammation in Glomerular Disease 10) Mitochondrial involvement in GN/NS 11) New Immunosuppressive Agents for GN/NS 12) IgA NephropathyConflict of Interest StatementAssistant Prof. Gabriel Cara-Fuentes has a pending patent application related to the therapeutic targeting of CD93 in nephrotic syndrome. The remaining editors declare no COI. Topic editors: George William Burke, Gabriel Cara-Fuentes Source: https://www.frontiersin.org/research-topics/71002/inflammation-immunity-and-autoimmunity-in-glomerulopathy-pre--and-post-transplant