Abstract
Immune-mediated glomerular disease is typified by membranous glomerulonephritis (MGN), lupus nephritis, and postinfectious glomerulonephritis (PIGN). Immune-mediated refers to the presence of immune complexes on a renal biopsy. The mechanisms responsible for formation and deposition of these complexes depend on the specific disease entity. However, once deposited, glomerular injury is mediated by both classical and alternative complement system activation and inflammatory cell recruitment. Animal models and large-scale genetic studies have significantly enhanced our understanding of the pathophysiological mechanisms underlying immune complex disease susceptibiLity and disease progression. However, it should be emphasized that animal models of MGN, lupus nephritis, and PIGN have significant flaws. A thorough understanding of the inflammatory mediators and genetic underpinnings of these diseases is critical to development of effective therapeutics and prevention strategies.
Original language | English |
---|---|
Title of host publication | Pathobiology of Human Disease |
Subtitle of host publication | A Dynamic Encyclopedia of Disease Mechanisms |
Publisher | Elsevier Inc. |
Pages | 2788-2801 |
Number of pages | 14 |
ISBN (Electronic) | 9780123864567 |
ISBN (Print) | 9780123864574 |
DOIs | |
State | Published - Jan 1 2014 |
Keywords
- Antinuclear antibodies
- Complement
- Hematuria
- Heymann nephritis
- Immune complex glomerulonephritis
- Lupus nephritis
- Membranous glomerulonephritis
- Postinfectious glomerulonephritis
- Proteinuria