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What type of immune complexes are formed in the glomeruli?
Which of the following accurately describes the location of large immune complexes?
In the context of glomerulonephritis, what does 'diffuse' refer to?
What causes proliferation or hypercellularity in the glomerular tuft?
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What characterizes crescent formation in glomerular disease?
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Which urinalysis test finding is most likely to be consistently present in patients with periorbital edema?
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What renal lesion is most likely present in a 5-year-old boy with periorbital edema and heavy proteinuria, who improves after corticosteroid therapy?
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Which form of glomerular disease is most likely in a 60-year-old man with malaise, pitting edema, and 4+ proteinuria, showing thickening of glomeruli on biopsy?
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In the context of renal disease, what finding is most indicative of chronic kidney damage?
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Which laboratory finding would suggest a possible urinary tract infection in patients with periorbital edema?
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What is the primary cause of nephrotic syndrome in adults?
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What histological feature is indicative of minimal change glomerulonephritis in electron microscopy?
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Which of the following is a common clinical feature of focal segmental glomerulosclerosis?
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In the pathogenesis of membranous glomerulonephritis, what type of immune complex is involved?
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What does FSGS stand for in terms of renal pathology?
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What is a notable response of minimal change disease to corticosteroid treatment?
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What is the primary characteristic of glomerulonephritis?
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What is a common age group for the incidence of minimal change disease?
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Which histological finding is associated with chronic stages of membranous glomerulonephritis?
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Which type of glomerulonephritis is characterized by heavy proteinuria exceeding 3.5 gm/24h?
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What is a common feature of nephritic syndrome?
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Which of the following is NOT classified under primary glomerulopathies?
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In the context of glomerular injury, which mechanism involves cytotoxic antibodies?
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What type of hypersensitivity is associated with circulating immune complex deposition in glomerulonephritis?
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Which disease is classified under nephritic syndrome?
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Which of the following statements about nephrotic syndrome is true?
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Which classification of glomerulonephritis is based on its duration?
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What is the predominant mechanism of pathogenesis in primary glomerulonephritis?
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Study Notes
Glomerulonephritis Definition
- Glomerular diseases in which the lesions are primarily in the glomeruli
- It is characterized by inflammation
- Absence of typical inflammation features
Glomerulonephritis Classification
- Classified according to cause, clinical presentation and duration
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Cause:
- Primary glomerulopathy: Intrinsic or unknown cause
- Secondary glomerulopathy: Resulting from other systemic diseases or conditions
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Clinical Presentation:
- Nephrotic syndrome: Massive proteinuria (>3.5 gm/24h), hypoalbuminemia (<3 gm), generalized edema, hyperlipidemia and lipiduria
- Nephritic syndrome: Hematuria, mild to moderate proteinuria, hypertension, oliguria, uremia, chronic renal failure
- Mixed: Features of both nephrotic and nephritic syndrome
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Duration:
- Acute glomerulonephritis: Rapid onset, often with a specific trigger
- Chronic glomerulonephritis: A long-term process, with gradual decline in kidney function
### Glomerulonephritis Specific Conditions
- Nephritic Syndrome: Diffuse proliferative glomerulonephritis, rapidly progressive glomerulonephritis (crescentic), Goodpasture syndrome, focal glomerulonephritis, Primary Berger's disease (IgA nephritis), Secondary IgA nephritis, Henoch-Schonlein purpura, Subacute bacterial endocarditis (SBE)
- Nephrotic Syndrome: Membranous glomerulonephritis, minimal changes glomerulonephritis, focal segmental glomerulosclerosis (FSGS), membranoproliferative glomerulonephritis, IgA nephropathy, secondary to systemic disease
Glomerulonephritis Pathogenesis
- Genetic: Congenital nephrotic syndrome
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Acquired:
- Immunological: Most forms of primary glomerulonephritis
- Non-immunological: Other factors such as drugs or toxins
Immune Mechanisms of Glomerular Injury
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Antibody-mediated injury:
- In situ immune complex deposition: Fixed tissue antigens, planted antigens
- Circulating immune complex deposition: Exogenous or endogenous antigens
- Cytotoxic antibodies
- Cell-mediated immune injury: T-cell mediated
- Activation of the alternative complement pathway: Independent of specific antibodies
Antibody-Mediated Injury
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Cytotoxic Antibodies (Antibodies to Glomerular Cells): Antibodies against glomerular cell antigens react with cellular components and cause injury by Type II hypersensitivity
- Antibodies to mesangial cell antigens: Mesangial cell proliferation
- Antibodies to endothelial cell antigens: Endothelial injury and intravascular thrombosis
- Antibodies to certain visceral epithelial cell proteins: Proteinuria
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Circulating Immune Complexes: Trapping of circulating antigen-antibody complexes within glomeruli (Type III hypersensitivity)
- Endogenous: RNA antigen, tumor antigen, unknown
- Exogenous: HBV, Streptococci, malaria, syphilis
- Site of deposition depends on size and molecular charges
- Small complexes tend to cross the GBM and reside subepithelially
- Large complexes are excluded from the GBM and trapped subendothelially
- Neutral charge complexes accumulate in the mesangium
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In situ Immune Complexes: Not seen in the circulation but formed within the glomeruli
- Fixed intrinsic tissue antigen: Examples include the capillary basement membrane (Goodpasture syndrome)
- Planted antigen: Antibodies react in situ with antigens not normally present in the glomerulus, but are "planted" there (e.g., bacteria)
### Histological Alterations and Descriptive Terms in Glomerulonephritis
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All Glomeruli:
- Diffuse: Involvement of ≥50% of the glomeruli
- Focal: Involvement of ≤50% of the glomeruli
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Individual Glomerulus:
- Global: If all or almost all of the glomerulus is affected
- Segmental: If only part of the glomerulus is affected
- Proliferation (Hypercellularity): Increase in the number of cells in the glomerular tuft
- Crescent formation (Partial epithelial proliferation): Accumulations of cells composed of proliferating parietal epithelial cells and infiltrating leukocytes
- Basement Membrane Thickening: Normal basement membrane structure is altered
- Sclerosis: Extracellular material deposition in the glomerulus similar in composition to the GBM and mesangial matrix
- Fibrosis: Deposition of collagen type I and III
### Nephrotic Syndrome
- Membranous glomerulonephritis (MGN): Major cause of nephrotic syndrome in adults, common in middle and old age, men > women
- Minimal Changes Glomerulonephritis (Lipoid Nephrosis): Major cause of nephrotic syndrome in children, common in 2-6 year olds
- Focal Segmental Glomerulosclerosis (FSGS): 80% present with nephrotic syndrome, focal = sclerosis of some glomeruli, not all, segmental = portion of the capillary tuft is affected
- Membranoproliferative glomerulonephritis: Features both nephrotic and nephritic syndrome
Membranous Glomerulonephritis
- Incidence: Major cause of nephrotic syndrome in adults, common in middle and old age, men > women
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Pathogenesis: In situ immune complex (IgG) along the wall of the glomeruli
- Primary: 85%, unknown antigen
- Secondary: Malignant tumor, drugs, infection
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Pathology:
- Light Microscopy: The glomeruli are more or less normal in size in early stages with no cellular infiltration or proliferation. Later stages show hyaline thickening in the glomerular basement membrane.
- Silver Stain: Thickening of the basement membrane with spikes.
- Electron Microscopy: Subepithelial irregular deposit of dense material in the basement membrane, thickening of the basement membrane, spikes in the basement membrane, effacement of podocytes, narrowing of capillary lumen leading to occlusion, hyalinization, atrophy of tubules and interstitial fibrosis in chronic stages
Minimal Changes Glomerulonephritis
- Incidence: Major cause of nephrotic syndrome in children, common in 2-6 year olds
- Pathogenesis: No immune deposits in the glomeruli, but an immunological basis is suggested
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Pathology:
- Light Microscopy: The glomeruli are more or less normal
- Electron Microscopy: Effacement of foot processes of podocytes replaced by a rim of cytoplasm with vacuolation. Proximal convoluted tubules are lipid-laden due to absorption of lipoproteins
- Clinical Course: Massive proteinuria (>3.5 gm, highly selective to albumin), renal function is normal, no hypertension or hematuria, dramatic response to corticosteroids, excellent prognosis
Focal Segmental Glomerulosclerosis
- Incidence: 80% present with nephrotic syndrome.
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Pathology:
- Light Microscopy: Sclerotic segments demonstrate collapsed basement membrane, increased mesangial matrix, hyalinization. Non-sclerotic segments appear more or less normal.
- Electron Microscopy: Diffuse effacement of foot processes, focal detachment of epithelial cells, denudation of basement membrane.
- Fate: Total sclerosis of glomeruli, tubular atrophy, interstitial fibrosis, chronic renal failure (CRF)
References
- https://www.clinicalkey.com/student/content/book/3-s2.0-B9780323531139000200#hl0001821
- https://www.clinicalkey.com/student/content/book/3-s2.0-B9780323531139000200#hl0001896
- https://www.clinicalkey.com/student/content/book/3-s2.0-B9780323531139000200#hl0002217
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Description
This quiz explores the definition and classification of glomerulonephritis, a type of kidney disease. Participants will learn about its causes, clinical presentations, and the differences between acute and chronic forms. This knowledge is essential for understanding kidney health and disease management.