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Year 2 > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

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
Q

What are the non-immunosuppressive means of GN treatment?

A

Hypertension control

  • ACE/ARB
  • Diuretic (oedema)
  • Statin (hyperlipidaemia)
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26
Q

What is the target blood pressure in someone with GN?

A
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27
Q

When might anticoagulants be used in GN?

A

Albumin

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28
Q

What are the immunosuppressive means of GN treatment?

A

Corticosteroids (prednisolone or IV methoprednisolone)
Azathioprine
Alkylating agents (cyclophosphamide)
Calcineurin inhibitors (cyclosporin, tacrolimus)
Mycophenolate mofetil

Plasmapharesis
Antibodies

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29
Q

How is nephrotic syndrome treated?

A 
Fluid and salt restrict
Diuretics
ACE/ARB
Anticoagulate if profoundly hypoalbumin
IV albumin if volume depletion 
Immunosuppression (steroids & another agent)
30
Q

Define the remission criteria of nephrotic syndrome

A

Proteinuria

31
Q

What are the main types of GN?

A 
Minimal change
Focal segmental glomerulosclerosis (FSGS)
Membranous
Membranoproliferative
IgA nephropathy
32
Q

What is the commonest cause of nephrotic syndrome in under 18s?

A

Minimal change nephropathy

33
Q

What is found in histological diagnosis of minimal change nephropathy?

A

Normal light microscopy
Normal immunofluorescence
Foot process fusion on electron microscopy

34
Q

How is minimal change nephropathy treated?

A

Oral steroids

Cyclophosphomide
CSA

35
Q

Minimal change nephropathy can rarely cause renal failure but only in under 5s. T/F

A

False - never causes renal failure

36
Q

Minimal change nephropathy is often steroid resistant. T/F

A

False - the minority are steroid resistant/have multiple relapses

37
Q

What is the suggested cause of minimal change nephropathy?

A

IL-13

38
Q

What is the commonest cause of GN in adults?

A

Focal segmental glomerulosclerosis

39
Q

List causes of secondary FSGS

A

HIV
Heroin
Obesity
Reflux nephropathy

40
Q

What is found on histological diagnosis of FSGS?

A

Characteristic appearance on light microscopy

Minimal Ig & complement deposition on immunofluorescence

41
Q

How is FSGS treated?

A

Steroids (prolonged)

Calcineurin inhibitors

42
Q

What percentage of patients with FSGS progress to renal failure?

A

50% over 10 years

43
Q

Describe the pathogenesis of FSGS

A

Increased soluble urokinase plasminogen activator receptors (suPAR) up-regulate integrins (cell signalling molecules) causing changes in podocytes

44
Q

Membraneous nephropathy can be primary or secondary. List some secondary causes

A

Infections (hep B, parasites)
Connective tissue diseases (lupus)
First manifestation of malignancy (lymphoma)
Drugs (gold, penicillamine i.e rheumatoid drugs)

45
Q

Most older adults with membraneous nephropathy have underlying malignancy. T/F

A

False - around 25%

46
Q

What is seen on renal biopsy of a patient with membraneous nephropathy?

A

Subepithelial immune complex deposition in the basement membrane

47
Q

How is membraneous nephropathy treated?

A

Steroids
Alkylating agents (cyclophosphamide)
B cell monoclonal antibodies (rituximab)

48
Q

Can membraneous nephropathy progress to end stage renal failure?

A

Yes - 30% do

49
Q

What is the cause of the majority of primary membraneous nephropathies?

A

Anti PLA2r antibody (on surface of podocytes)

50
Q

What is characteristically seen histologically in membranous nephropathy?

A

Thickened basement membrane (silver stain)

51
Q

What is the commonest nephropathy world wide?

A

IgA nephropathy

52
Q

How does IgA nephropathy present?

A
  • Asymptomatic haematuria +/- non nephrotic range proteinuria
  • Macroscopic haematuria post resp/GI infection
  • AKI
  • CKD
53
Q

What conditions are associated with IgA nephropathy?

A

Henoch-Schonlein purpura (arthritis, colitis, purpuric rash)

54
Q

How does IgA appear on renal biopsy?

A

Mesangeal cell proliferation and expansion on light microscopy
IgA deposits in mesangium on immunofluorescence

55
Q

Can IgA nephropathy progress to end stage renal failure?

A

Yes - 25% do (10-30 years timescale)

56
Q

How is IgA nephropathy treated?

A

ACE/ARB (i.e BP control)

57
Q

How does IgA nephropathy look histologically?

A

Increased mesangeal cells (increased purple dots!)

58
Q

How does rapidly progressive glomerulonephritis (RPGN) present?

A 
Rapid deterioration in renal function over days/weeks
Urinary sediment (RBC, granular casts)
\+/- systemic disease
59
Q

What is found on biopsy of someone with RPGN?

A

Crescents

60
Q

What does ANCA stand for?

A

Anti neutrophil cytoplasmic antibody

61
Q

How can RPGN be classified?

A

ANCA positive

ANCA negative

62
Q

What are some causes of ANCA positive RPGN?

A

GPA

Microscopic polyangitis

63
Q

What are some causes of ANCA negative RPGN?

A

Goodpastures disease
Henloch scholein purpura (systemic IgA nephropathy)
Lupus

64
Q

Which antibody is present in goodpastures disease?

A

Anti glomerular basement membrane (anti-GBM)

65
Q

How is ANCA tested?

A

Indirect immunofluorescence

66
Q

What happens to blood vessels at end stage vasculitis? What does this result in within the kidney?

A

Endothelial rupture

Crescent formation on histology

67
Q

By which processes are acellular fibrous crescents formed with respect to RPGN?

A

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
Q

How does vasculitis manifest dermatologically?

A

Vasculitic skin rash aka purpura

69
Q

Give another name for Goodpasture’s syndrome

A

Pulmonary-renal syndrome

70
Q

How does goodpasture’s syndrome present?

A

Pulmonary haemorrhage (i.e coughing up blood) + renal failure

71
Q

How is RPGN treated?

A

Strong immunosuppression +/- renal support (i.e dialysis)

72
Q

Which immunosuppresants can be used in RPGN?

A

Steroids (IV methypred 3 days –> oral pred) +
Cyclophosphamide OR rituximab
Plasmapharesis (advanced renal failure)

Year 2 (72 decks)

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