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Questions and Answers
What role do CD4+ T lymphocytes play in glomerular injury?
What role do CD4+ T lymphocytes play in glomerular injury?
Which of the following is a deposition disease linked to glomerular injury?
Which of the following is a deposition disease linked to glomerular injury?
What is a major consequence of intraglomerular hypertension during end-stage renal failure?
What is a major consequence of intraglomerular hypertension during end-stage renal failure?
Which cells are primarily implicated in antibody-dependent cell toxicity leading to glomerular cell injury?
Which cells are primarily implicated in antibody-dependent cell toxicity leading to glomerular cell injury?
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What is a characteristic feature of nephrotoxic infectious diseases affecting the glomeruli?
What is a characteristic feature of nephrotoxic infectious diseases affecting the glomeruli?
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Which of the following mechanisms is characterized as secondary pathogenesis in glomerular injury?
Which of the following mechanisms is characterized as secondary pathogenesis in glomerular injury?
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Why are neutrophils significant in certain forms of glomerular disease?
Why are neutrophils significant in certain forms of glomerular disease?
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What is the final outcome of progressive glomerulosclerosis if left unchecked?
What is the final outcome of progressive glomerulosclerosis if left unchecked?
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What primarily mediates the immunologic mechanisms underlying glomerular injury?
What primarily mediates the immunologic mechanisms underlying glomerular injury?
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What condition is indicated by asymptomatic hematuria in the context of glomerular diseases?
What condition is indicated by asymptomatic hematuria in the context of glomerular diseases?
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Which of the following cell types is responsible for maintaining glomerular perfusion?
Which of the following cell types is responsible for maintaining glomerular perfusion?
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What is a potential consequence of injury to mesangial cells?
What is a potential consequence of injury to mesangial cells?
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Asymptomatic proteinuria in a patient can be indicative of which underlying condition?
Asymptomatic proteinuria in a patient can be indicative of which underlying condition?
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Which of the following is NOT associated with asymptomatic hematuria?
Which of the following is NOT associated with asymptomatic hematuria?
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Which consequence is expected from injury to visceral epithelial cells?
Which consequence is expected from injury to visceral epithelial cells?
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What role do endothelial cells play in glomerular function?
What role do endothelial cells play in glomerular function?
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What role do neutrophils play in glomerular injury?
What role do neutrophils play in glomerular injury?
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Which of the following is a mechanism identified in antibody-mediated glomerular injury?
Which of the following is a mechanism identified in antibody-mediated glomerular injury?
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What is the significance of mononuclear phagocyte accumulation in glomerular diseases?
What is the significance of mononuclear phagocyte accumulation in glomerular diseases?
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What does the activation of the complement system lead to in the context of glomerular injury?
What does the activation of the complement system lead to in the context of glomerular injury?
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Which factor is implicated in the pathogenesis of glomerular injury aside from antibodies?
Which factor is implicated in the pathogenesis of glomerular injury aside from antibodies?
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Which of the following statements about cell-mediated immunity and glomerular injury is accurate?
Which of the following statements about cell-mediated immunity and glomerular injury is accurate?
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What is C5bC6789 known for in the context of glomerular diseases?
What is C5bC6789 known for in the context of glomerular diseases?
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In what forms of glomerular diseases are autoantibodies such as ANCA and AECA implicated?
In what forms of glomerular diseases are autoantibodies such as ANCA and AECA implicated?
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Study Notes
Glomerular Injury
- Neutrophils cause glomerular injury via activation of complement and release of proteases, arachidonic acid metabolites, and oxygen-derived free radicals.
- These agents degrade the glomerular basement membrane (GBM) and cause cell injury.
Mononuclear Phagocytes
- Monocytes and macrophages infiltrate glomeruli in many cases of human and experimentally induced proliferative glomerulonephritis (GN).
- Their accumulation contributes to hypercellularity alongside mesangial and endothelial cell proliferation.
- Activated macrophages release various biologically active substances contributing to glomerular injury.
Complement System
- The classical and alternate pathways of complement activation contribute to glomerular injury.
- Complement components, such as the membrane attack complex (MAC; C5b-9), directly damage the GBM.
T Lymphocytes
- CD4+ T lymphocytes recruit macrophages.
- CD8+ cytotoxic T lymphocytes and natural killer cells contribute to glomerular cell injury via antibody-dependent cell toxicity.
Pathogenesis of Glomerular Diseases
- Most human glomerular diseases have immunologic pathogenesis, either antibody-mediated or cell-mediated.
- Antibody-mediated glomerular injury involves immune complexes and specific autoantibodies like anti-GBM antibodies, anti-neutrophil cytoplasmic antibodies (ANCAs), and anti-endothelial cell antibodies (AECAs).
- Cell-mediated immune reactions, such as delayed-type hypersensitivity, can also cause glomerular injury.
- Secondary mechanisms involve neutrophils, monocytes, complement, platelets, mesangial cells, and the coagulation system.
- Non-immunologic mechanisms play a role in certain metabolic, infiltrative, and inherited glomerular diseases.
Secondary Pathogenetic Mechanisms (Mediators of Immunologic Injury )
- Neutrophils are prominent in certain forms of GN, including acute diffuse proliferative GN, membranoproliferative GN, and lupus nephritis.
- Systemic hypertension and intraglomerular hypertension in focal segmental glomerulosclerosis (FSGS) contribute to end-stage renal failure.
- Adaptive glomerular hypertrophy of unaffected glomeruli leads to increased glomerular blood flow, glomerular capillary pressure, and intraglomerular hypertension, ultimately causing mesangial matrix deposition, mesangial cell proliferation, endothelial and epithelial cell injury, and progressive glomerulosclerosis.
Immunologic Mechanisms
- Antibody-mediated mechanisms primarily involve immune-complex disease.
- Cell-mediated immune reactions, such as delayed-type hypersensitivity, may also contribute to glomerular injury.
Asymptomatic Proteinuria
- Presence of proteinuria without clinical symptoms may indicate mild glomerulonephritis or be unrelated to renal disease.
- Asymptomatic proteinuria with hematuria, hypertension, or impaired renal function suggests underlying glomerulonephritis.
Asymptomatic Hematuria
- Asymptomatic microscopic hematuria is common in children and adolescents and can have various causes including diseases of the urinary tract.
Physiologic Role of Glomerular Components and Consequences of Injury
- Endothelial cells maintain glomerular perfusion, prevent leukocyte adhesion and platelet aggregation.
- Injury to endothelial cells leads to vasoconstriction, leukocyte infiltration, and intravascular microthrombi.
- Mesangial cells control glomerular filtration, and their injury leads to proliferation and increased matrix deposition.
- Visceral epithelial cells prevent plasma protein filtration, and their injury results in proteinuria.
Glomerular Disease Types
- Proliferative GN: Characterized by proliferation of glomerular cells.
- Membranoproliferative GN: Thickening of the glomerular basement membrane and mesangial expansion.
- Minimal Change Disease (MCD): Characterized by foot process effacement in podocytes.
- Focal Segmental Glomerulosclerosis (FSGS): Scarring in some glomeruli.
Non-Immunologic Mechanisms
- Systemic Hypertension: Can exacerbate existing kidney damage.
- Intraglomerular Hypertension: Increases pressure within the glomerulus, leading to injury.
- Deposition Diseases: e.g., amyloidosis.
- Infectious Diseases: e.g., Hepatitis B virus (HBV), Hepatitis C virus (HCV), Human immunodeficiency virus (HIV), Escherichia coli (E. coli)-derived nephrotoxin.
- Drugs: e.g., Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause MCD.
- Inherited Glomerular Diseases: e.g., Alport syndrome, nail-patella syndrome.
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Description
Explore the mechanisms of glomerular injury caused by various immune cells. Understand how neutrophils, mononuclear phagocytes, and T lymphocytes contribute to injury in glomerulonephritis. This quiz covers the roles of the complement system and macrophage activation in glomerular damage.
