Immune-mediated glomerulopathy in children represents a significant subset of pediatric renal diseases, characterized by inflammation and damage to the glomeruli due to aberrant immune responses. The pathogenesis involves genetic susceptibility, environmental factors, and immune dysregulation. Key mechanisms include immune complex formation and deposition in the glomeruli, autoantibody production against intrinsic glomerular antigens, and activation of the complement system. These events lead to glomerular injury via inflammatory cell infiltration, cytokine and chemokine release, and direct damage to cellular and extracellular matrix components.

In children, the most common forms include minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and membranoproliferative glomerulonephritis (MPGN) and complement mediated glomerulopathies. Pediatric immune-mediated glomerulopathies often present with nephrotic syndrome, characterized by proteinuria, hypoalbuminemia, and edema. The role of T and B lymphocytes, as well as various cytokines and signaling pathways, has been increasingly recognized in the pathogenesis of these conditions.

Advances in understanding these mechanisms have led to the development of targeted therapies, including immunosuppressive agents and biologics that modulate specific components of the immune system. This research focuses on the immunopathogenic processes in pediatric immune-mediated glomerulopathy, emphasizing the distinct aspects of disease presentation, progression, and treatment in children