Heymann nephritis is an experimental autoimmune model of nephritis that mimics human membranous nephropathy. It is induced by immunization with a protein found in the glomerular basement membrane, leading to the formation of immune complexes that deposit in the glomeruli.
Step 1: Pathogenesis of Heymann Nephritis:
1. Immunization: The model is induced in animals, typically rats, by injecting them with a renal antigen (megalin) extracted from the proximal tubular cells of the kidneys. The immune response to this antigen leads to the formation of antibodies.
2. Immune Complex Deposition: The antibodies formed against the antigen bind to the glomerular basement membrane, forming immune complexes. These complexes deposit along the glomerular capillaries, triggering an inflammatory response.
3. Inflammation and Proteinuria: The immune complexes activate complement and attract inflammatory cells, leading to glomerular injury, which results in proteinuria and nephrotic syndrome in the animal model.
Step 2: Clinical Relevance:
1. Human Relevance: Heymann nephritis serves as a model for human membranous nephropathy, a condition characterized by thickening of the glomerular basement membrane and the presence of immune complexes.
2. Use in Research: The model helps to study the pathogenesis of glomerular diseases and test potential therapeutic interventions for treating nephrotic syndrome and autoimmune renal diseases.