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Glomerulonephritis Flashcards

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1
Q

Which parts of the renal parenchyma can be affected in renal disease?

A

Tubules
Interstitium
Glomeruli

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2
Q

What are some glomerular disease?

A

Diabetic nephropathy
Glomerulonephritis
Amyloid/light chain nephropathy
Transplant glomerulopathy

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3
Q

How can glomerulonephritis be divided? Which is more common?

A

Chronic (common)

Acute

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4
Q

What is glomerulonephritis?

A

Immune mediated disease affecting the glomeruli +/- secondary tubulointerstitial damage

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5
Q

What are the three mediators of glomerulonephritis?

A

Antibodies (humeral) & immune complexes
Cells (T cells)
Inflammatory cells/mediators/complement

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6
Q

How can antibody induced glomerulonephritis be further subdivided?

A

Intrinsic

Planted (circulating antigen that has become stuck in glomerulus)

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7
Q

Glomerular capillaries are fenestrated. T/F

A

True

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8
Q

How is proteinuria and haematuria caused in glomerulonephritis?

A

Disruption of the basement membrane

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9
Q

Which features must solutes have in order to cross the glomerular membrane?

A

Small

Positively charged

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10
Q

Describe proliferative and non-proliferative GN and the differences in it’s clinical presentation

A

Proliferative - endothelial and/or mesangeal cell damage allowing red cells to pass into the urine
Non-proliferative - podocyte damage allowing protein to pass into the urine

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11
Q

What does urine microscopy look for?

A

Red blood cells, granular casts and lipids

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12
Q

How can urine protein be measured?

A

Protein creatinine ratio

24 hr urinary collection

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13
Q

In which two ways can haematuria present?

A

Asymptomatic microscopic

Painless macroscopic

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14
Q

What do dysmorphic red blood cells indicate?

A

They originated from the kidney (because they passed through glomerular membrane)

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15
Q

How might renal disease present?

A

Haematuria
Proteinuria
Hypertension
Impaired renal function (AKD/CKD)

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16
Q

How does nephritic syndrome present? What does it indicate?

A 
AKI
Oedema
Oliguria
Hypertension
Sediment (RBC, granular casts)

Proliferative process (endothelial)

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17
Q

How does nephrotic syndrome present? What does it indicate?

A 
Proteinuria >3g
Hypoalbuminuria
Odema
Hypercholesterolaemia 
Normal renal function

Non-proliferative process (epithelial)

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18
Q

What are the complications of nephrotic syndrome? Explain each one

A

Infection risk (loss of Ig proteins)
Renal vein thrombosis (shift in liver production of pro-thombotic factors)
Pulmonary emboli
Volume depletion (too much diuretic) –> AKI
Vitamin D deficiency
Subclinical hypothyroidism

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19
Q

In which two methods might glomerulonephritis be classified?

A

Aetiology based

Histologically

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20
Q

What are the causes of glomerulonephritis?

A 
Idiopathic
Infection
Drugs
Malignancies 
Systemic disease (e.g ANCA associated)
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21
Q

By which methods can glomerulonephritis be histologically classified?

A

Biopsy
Microscopy
Immunofluroscence
Electron microscopy

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22
Q

What are the histological classifications of GN?

A

Proliferative/non-proliferative (mesangial/inflamm cells)
Focal/diffuse (>50% affected)
Global/segmental (all or part of glomeruli)
Crescentic (extracapillary proliferation of cells in bowman;s space)

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23
Q

When would you find crescentic injury?

A

Vasculitic GN (rapidly progressing)

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24
Q

What are the two methods of glomerulonephritis treatment?

A

Immunosuppressive and non immunosuppressive

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25
What are the non-immunosuppressive means of GN treatment?
Hypertension control - ACE/ARB - Diuretic (oedema) - Statin (hyperlipidaemia)
26
What is the target blood pressure in someone with GN?
27
When might anticoagulants be used in GN?
Albumin
28
What are the immunosuppressive means of GN treatment?
Corticosteroids (prednisolone or IV methoprednisolone) Azathioprine Alkylating agents (cyclophosphamide) Calcineurin inhibitors (cyclosporin, tacrolimus) Mycophenolate mofetil Plasmapharesis Antibodies
29
How is nephrotic syndrome treated?
``` Fluid and salt restrict Diuretics ACE/ARB Anticoagulate if profoundly hypoalbumin IV albumin if volume depletion Immunosuppression (steroids & another agent) ```
30
Define the remission criteria of nephrotic syndrome
Proteinuria
31
What are the main types of GN?
``` Minimal change Focal segmental glomerulosclerosis (FSGS) Membranous Membranoproliferative IgA nephropathy ```
32
What is the commonest cause of nephrotic syndrome in under 18s?
Minimal change nephropathy
33
What is found in histological diagnosis of minimal change nephropathy?
Normal light microscopy Normal immunofluorescence Foot process fusion on electron microscopy
34
How is minimal change nephropathy treated?
Oral steroids Cyclophosphomide CSA
35
Minimal change nephropathy can rarely cause renal failure but only in under 5s. T/F
False - never causes renal failure
36
Minimal change nephropathy is often steroid resistant. T/F
False - the minority are steroid resistant/have multiple relapses
37
What is the suggested cause of minimal change nephropathy?
IL-13
38
What is the commonest cause of GN in adults?
Focal segmental glomerulosclerosis
39
List causes of secondary FSGS
HIV Heroin Obesity Reflux nephropathy
40
What is found on histological diagnosis of FSGS?
Characteristic appearance on light microscopy | Minimal Ig & complement deposition on immunofluorescence
41
How is FSGS treated?
Steroids (prolonged) | Calcineurin inhibitors
42
What percentage of patients with FSGS progress to renal failure?
50% over 10 years
43
Describe the pathogenesis of FSGS
Increased soluble urokinase plasminogen activator receptors (suPAR) up-regulate integrins (cell signalling molecules) causing changes in podocytes
44
Membraneous nephropathy can be primary or secondary. List some secondary causes
Infections (hep B, parasites) Connective tissue diseases (lupus) First manifestation of malignancy (lymphoma) Drugs (gold, penicillamine i.e rheumatoid drugs)
45
Most older adults with membraneous nephropathy have underlying malignancy. T/F
False - around 25%
46
What is seen on renal biopsy of a patient with membraneous nephropathy?
Subepithelial immune complex deposition in the basement membrane
47
How is membraneous nephropathy treated?
Steroids Alkylating agents (cyclophosphamide) B cell monoclonal antibodies (rituximab)
48
Can membraneous nephropathy progress to end stage renal failure?
Yes - 30% do
49
What is the cause of the majority of primary membraneous nephropathies?
Anti PLA2r antibody (on surface of podocytes)
50
What is characteristically seen histologically in membranous nephropathy?
Thickened basement membrane (silver stain)
51
What is the commonest nephropathy world wide?
IgA nephropathy
52
How does IgA nephropathy present?
- Asymptomatic haematuria +/- non nephrotic range proteinuria - Macroscopic haematuria post resp/GI infection - AKI - CKD
53
What conditions are associated with IgA nephropathy?
Henoch-Schonlein purpura (arthritis, colitis, purpuric rash)
54
How does IgA appear on renal biopsy?
Mesangeal cell proliferation and expansion on light microscopy IgA deposits in mesangium on immunofluorescence
55
Can IgA nephropathy progress to end stage renal failure?
Yes - 25% do (10-30 years timescale)
56
How is IgA nephropathy treated?
ACE/ARB (i.e BP control)
57
How does IgA nephropathy look histologically?
Increased mesangeal cells (increased purple dots!)
58
How does rapidly progressive glomerulonephritis (RPGN) present?
``` Rapid deterioration in renal function over days/weeks Urinary sediment (RBC, granular casts) +/- systemic disease ```
59
What is found on biopsy of someone with RPGN?
Crescents
60
What does ANCA stand for?
Anti neutrophil cytoplasmic antibody
61
How can RPGN be classified?
ANCA positive | ANCA negative
62
What are some causes of ANCA positive RPGN?
GPA | Microscopic polyangitis
63
What are some causes of ANCA negative RPGN?
Goodpastures disease Henloch scholein purpura (systemic IgA nephropathy) Lupus
64
Which antibody is present in goodpastures disease?
Anti glomerular basement membrane (anti-GBM)
65
How is ANCA tested?
Indirect immunofluorescence
66
What happens to blood vessels at end stage vasculitis? What does this result in within the kidney?
Endothelial rupture | Crescent formation on histology
67
By which processes are acellular fibrous crescents formed with respect to RPGN?
Vasculitic inflammation causes endothelial rupture allowing blood and inflammatory cells to leak out --> Leakage gradually compresses glomerulus until it becomes ischaemic --> Develops into fibrous remanent
68
How does vasculitis manifest dermatologically?
Vasculitic skin rash aka purpura
69
Give another name for Goodpasture's syndrome
Pulmonary-renal syndrome
70
How does goodpasture's syndrome present?
Pulmonary haemorrhage (i.e coughing up blood) + renal failure
71
How is RPGN treated?
Strong immunosuppression +/- renal support (i.e dialysis)
72
Which immunosuppresants can be used in RPGN?
Steroids (IV methypred 3 days --> oral pred) + Cyclophosphamide OR rituximab Plasmapharesis (advanced renal failure)

Year 2 (72 decks)

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