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3 - Pathology > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What is a normal glomerulus?

A

A vascular structure formed of an anastomosing network of capillaries that arise from the afferent arteriole and then drain into the efferent arteriole

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2
Q

What does the tuft of capillaries lie within?

A

Lumen of the Bowman Capsule

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3
Q

Where does plasma ultrafiltrate (urine) collect?

A

Bowman Space (urinary space)

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4
Q

What lines Bowman’s Space?

A

Parietal epithelium

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5
Q

What lines the outside of the capillary wall?

A

Visceral epithelium (composed of podocytes)

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6
Q

What does the glomerular capillary wall consist of?

A

A thin layer of fenestrated endothelial cells
A glomerular basement membrane (GBM)
Podocytes with their foot process adherent to outside the BM
Mesangial cells that support the glomerular tuft. These lie between the capillaries; scattered in a basement membrane-like material called mesangial matrix or mesangium.

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7
Q

What is the main barrier of the glomerulus preventing albumin filtration?

A

Podocytes are the main barrier against albumin filtration

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8
Q

What is the function of the glomerular capillary wall?

A

Filtration barrier with selective permeability (depends on size and charge of filtering molecules)

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9
Q

Name the two types of antibody and immune complex mediated injury causing glomerulonephritis.

A

In situ (in the glomerulus) deposition of antibodies with or without immune complex formation (types III and II hypersensitivity)

Circulating (the immune complex is circulating in blood and becomes trapped in the glomerulus) immune complex deposition (type III hypersensitivity)

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10
Q

How do we detect antibodies/immune complexes?

A

Via immunofluorescence
Antibodies to various immunoglobulins and complement components are used; linked to a fluorescent dye and examined microscopically under UV light

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11
Q

Describe the two patterns of immunofluorescence.

A

Granular: circulating and in situ immune complex. Haphazard deposition in several types of GN.
Linear: anti-glomerular basement membrane (anti-GBM) antibody glomerulonephritis (GBM - a linear structure - will be highlighted by antibodies against its components)

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12
Q

List locations of immune complexes in the glomerulus.

A

Subepithelial deposits
Subendothelial deposits
Mesangial deposits
Basement membrane deposits

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13
Q

What does the location of immune complex deposition in the glomerulus depend on?

A

Size and charge

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14
Q

Describe the mechanism of glomerular injury after antibody binding or immune complex deposition.

A

1 - complement activation leading to leucocyte recruitment, inflammation and tissue injury
2 - recruitment of leucocytes by engagement of Fc receptor on their surface to Fc portion of antibodies

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15
Q

Poststreptococcal Glomerulonephritis - when does it show up and who does it affect?

A

Appears 1 to 4 weeks following skin or pharyngeal infection by nephritogenic strains of group A beta hemolytic streptococci
Mainly affects children aged 6 to 10

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16
Q

What causes poststreptococcal glomerulonephritis?

A

Immune complex deposition (unclear whether circulating or in situ) in subendothelial location = complement activation and inflammation
Inflammatory mediators = proliferation of endothelial mesangial cells and infiltration by leukocytes

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17
Q

What antigens are incriminated in the pathogenesis of poststreptococcal glomerulonephritis?

A

Streptococcal pyogenic exotoxin B (SpeB)

Streptococcal glyceraldehyde-3-phosphate dehydrogenase (GAPDH)

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18
Q

Clinical presentation of poststreptococcal glomerulonephritis.

A

Acute onset of fever, malaise and nausea (flu-like symptoms)
Nephritic Syndrome (Syndrome of Acute Nephritis):
- oliguria - decreased amount of urine due to reduction in GFR
- hematuria - smoky/cola coloured urine: inflammatory damage to capillary walls with leakage of RBCs
- mild proteinuria
- mild to moderate HTN

Elevated titers of anti-streptococcal antibodies and low serum levels of C3 (consumption of complement components)

In children: recovery is the rule

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19
Q

Light microscopy of poststreptococcal glomerulonephritis.

A

Enlarged, hypercellular glomeruus
Obliterated capillary lumens
Increased cellularity due to cellular proliferation and leukocytic infiltration

20
Q

Electron microscopy of poststreptococcal glomerulonephritis.

A

Sub epithelial electron dense immune complex deposits (humps)

21
Q

Where do immune complexes first deposit?

A

Subendothlial location

Then they dissociate, migrate across GBM and reform in a supepithelial location

22
Q

Immunofluorescence of poststrep glomerulonephritis.

A

Granular (bumpy) deposits of IgG, IgM and C3 complement protein

23
Q

Crescentic Glomerulonephritis (RPGN)

A

Associated with severe glomerular injury
Rapid loss of renal function
Nephritic syndrome

May be caused by a number of diseases

Characterized histologically by presence of crescents within the glomerulus

24
Q

What are red cell casts?

A

Cylindrical shaped aggregates of red cells bound together by Tamm-Horsfall mucoprotein secreted by the renal tubular cells

25
What is the importance of casts?
Distinguishing primary renal disease from disease of the lower urinary tract
26
Name the three types of crescentic glomerulonephritis (RPGN)
Type I: Anti-glomerular basement membrane antibody Type II: Immune complex mediated Type III: Pauci-immune
27
What is goodpasture syndrome?
Anti-GBM antibodies cross react with pulmonary alveolar BM leading to pulmonary haemorrhage in addition to renal failure
28
Immunofluorescence pattern of Type I, type II and type III RPGN.
Linear in type I Granular in type II Type III - no immune deposits
29
What is the pathogenesis behind RPGN?
Disruption of the capillary BM allows leakage of fibrinogen into the urinary space and deposition of fibrin Fibrin deposition, along with inflammatory mediators induces proliferation of parietal epithelial cells and influx of macrophages resulting in crescent formation
30
Light microscopy of RPGN
Collapsed capillary tufts Crescents of proliferated parietal epithelial cells, monocytes and fibrin strands are seen agains the Bowman's capsule Crescents become fibrosed over time
31
Electron microscopy of RPGN
Wrinkled, focally disrupted glomerular basement membrane
32
Immunofluorescence of RPGN
Linear pattern of IgG positivity along the capillary BM | Tuft is compressed by an epithelial crescent
33
What is the outcome of RPGN?
Progressive decline in renal function End stage kidney disease if left untreated Recovery may follow therapy by plasmapheresis, steroids and cytotoxic agents in Goodpasture syndrome Other forms of RPGN may respond to steroids and cytotoxic therapy
34
Nephrotic Syndrome features
Massive proteinuria >3.5gm/day (mainly albumin is lost in urine) Hypoalbuminaemia (massive loss in urine) Generalized edema (decreased intravascular osmotic pressure) Hyperlipidemia and lipiduria (complex mechanism - perhaps increased synthesis in liver, abnormal transport in plasma, decreased catabolism)
35
Pathophysiology of Nephrotic Syndrome
Increased permeability of glomerular capillary wall to plasma proteins due to alterations in the structural components of the glomerular filtration barrier - mainly podocytes which are the main barrier against albumin filtration Classically seen in non-inflammatory glomerular diseases
36
Causes of nephrotic syndrome
Primary glomerular disease | Systemic diseases affecting the kidney
37
What are examples of primary glomerular disease?
Membranous nephropathy | Minimal change glomerulopathy
38
What is minimal change glomerulopathy?
Most frequent cause of nephrotic syndrome in children May follow vaccination or resp tract infection No histological changes seen by light microscopy No immune complex deposits seen Only change seen in EM is effaced (erased) podocyte foot processes Responds well to steroids
39
What are systemic diseases affecting the kidney?
Diabetes mellitus - podocyte injury is now believed to be the main cause of albuminuria in diabetes, in addition to endothelial dysfunction Amyloidosis Systemic lupus erythematosus (SLE) Other: NSAIDs, infections (Hep B, C, HIV), malignancy
40
What causes membranous nephropathy?
75% of cases are primary (HLA-related autoimmune disease against phospholipase A2 receptor [PLA2R] on podocytes) Secondary causes occur in association with certain drugs (NSAIDs), malignancy, SLE, infections such as hepatitis etc. Caused by accumulation of IgG containing immune complex deposits in subepithelial location. These ultimately become incorporated into the BM leading to its thickening.
41
What causes protein leakage in membranous nephropathy?
C5b-C9 MAC activates the podocytes which release proteolytic enzymes and lose their foot processes This damages the filtration barrier
42
Light microscopy membranous nephropathy
Increase in thickness of glomerular capillary walls throughout the glomerulus with no increase in glomerular cellularity or inflammatory infiltration
43
Why does membranous nephropathy cause no increase in cells/inflammatory infiltration?
No inflammatory cells recruited or cellular proliferation in the glomerulus - complement has no access to inflammatory cells as they are not on the capillary side of BM
44
Electron microscopy - membranous nephropathy
Thickened basement membrane | Immune complex deposits incorporated into the BM account for the spiked appearance under light microscopy
45
Light microscopy of end stage kidney disease
Most glomeruli are sclerotic Tubules are atrophic and contain protein (hyaline) casts Lymphocytic infiltrate
46
What is the function of a renal biopsy?
Obtain a core of renal tissue and send it to pathology
47
How do we diagnose glomerular diseases.
Clinical presentation and lab results | Renal biopsy - light microscopy, electron microscopy, immunofluorescence, immunohistochemistry

3 - Pathology (7 decks)

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