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Renal 09 Glom. Dz
Dickinson: Glomerular disease - introduction
Question | Answer |
---|---|
Most glomerular diseases are... | Immune mediated |
Which immune systems mediate glomerular injury? | Innate and adaptive |
Immune-mediated injury occurs through... | Inflammatory and non-inflammatory mechanisms |
Classification of glomerular disease | 1. Nephrotic/Nephritic 2. Proliferative, sclerotic or membranous 3. Primary or secondary |
Classification of glomerular disease: Proliferative | Increase in cellular components of the glomerulus regardless of origin |
Classification of glomerular disease: Sclerotic | Increase in the non-cellular components of the glomerulus |
Classification of glomerular disease: Membranous | Increase in the thickness of the glomerular capillary wall Often caused by immune complex deposition |
Classification of glomerular disease: Primary V Secondary | Primary -Kidneys are directly affected Secondary -Kidneys are damaged as a result of systemic disease, toxin or medication |
Nephrotic Syndrome | Increased permeability Protein loss Proteinuria >3.5 g/day Non-inflammatory |
Nephritic syndrome | Inflammatory process Hematuria Low proteinuria Decreases permeability of the GCW |
Glomerular capillary wall (4 layers) | Mesangial cells Endothelium GBM Podocytes |
Immune complexes can be found in.. | Mesangium Subendothelium Basement membrane Subepithelium |
Immune complexes of antibodies form with ____ or ____ | Fixed glomerular antigens Exogenous non-renal antigens |
Type of glomerular lesion depends on.. | Site of immune complex deposition |
Site of deposition determines... | What mediators of tissue injury are activated |
In situ immune complex deposition: Ab binding to... | Endogenous renal antigen Endogenous non-renal antigen Exogenous antigen |
Preformed circulating immune complex deposition | Preformed complexes re transported directly to kidney tissue via the circulation and trapped -Lupus -Post-group A strep infxn |
Nephrotic syndrome: Target of injury and site of complex depostion | Podocytes Subepithelial complexes |
Nephrotic syndrome: Activates... | Membrane attack complex |
Which complement pathway is initiated by IgG? | Classical |
Classical complement pathway | Recruits neutrophils, monocytes, macrphages Produces MAC which damages podocytes |
Non-inflammatory mechanism of classical pathway | Does not recruit cells MAC damages podocytes |
Non-inflammatory mechanism for subendothelial immune complex deposition | Phagocytes can't cross GBM Chemoattractants can't establish a gradient |
Nephritic syndrome | Immune complex deposition in mesangium and subendothelium Immune cells cause tissue damage MAC produced |
Inflammatory classical pathway | Recruits neutrophils, monocytes, macrphages Produces MAC which damages membranes |
What serum proteins accumulate in tissues during an inflammatory response? | Growth factors Albumin Chemokines |
How do complexes cause glomerular injury? | 1. Activate complement 2. Chemokines recruit macrophages and neutrophils 3. MAC injures plasma membranes 4. phagocytes activated |
How do complexes cause glomerular injury? (cont.) | 5. Phagocytes produce pro-inflammatory mediators, ROS, lysosomal enzymes and proteases |
IgA Nephropathy | Most frequent form of idiopathic glomerularnephritis worldwide Deposition of IgA in mesangium Induces inflammation |
IgA nephropathy: Pathogenesis | Abnormal gylcosylation of IgA Induces self aggregation |
IgA nephropathy: Nephritic syndrome | Glycosylated dimeric IgA activates the Lectin complement pathway Induces MAC production Microscopic hematuria in the absence of sustained proteinuria |
IgA nephropathy: Dx | Made by immunofluorescence of IgA |