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Flashcards in Glomerulonephritis Deck (72):
1

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

Tubules
Interstitium
Glomeruli

2

What are some glomerular disease?

Diabetic nephropathy
Glomerulonephritis
Amyloid/light chain nephropathy
Transplant glomerulopathy

3

How can glomerulonephritis be divided? Which is more common?

Chronic (common)
Acute

4

What is glomerulonephritis?

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

5

What are the three mediators of glomerulonephritis?

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

6

How can antibody induced glomerulonephritis be further subdivided?

Intrinsic
Planted (circulating antigen that has become stuck in glomerulus)

7

Glomerular capillaries are fenestrated. T/F

True

8

How is proteinuria and haematuria caused in glomerulonephritis?

Disruption of the basement membrane

9

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

Small
Positively charged

10

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

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

11

What does urine microscopy look for?

Red blood cells, granular casts and lipids

12

How can urine protein be measured?

Protein creatinine ratio
24 hr urinary collection

13

In which two ways can haematuria present?

Asymptomatic microscopic
Painless macroscopic

14

What do dysmorphic red blood cells indicate?

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

15

How might renal disease present?

Haematuria
Proteinuria
Hypertension
Impaired renal function (AKD/CKD)

16

How does nephritic syndrome present? What does it indicate?

AKI
Oedema
Oliguria
Hypertension
Sediment (RBC, granular casts)

Proliferative process (endothelial)

17

How does nephrotic syndrome present? What does it indicate?

Proteinuria >3g
Hypoalbuminuria
Odema
Hypercholesterolaemia
Normal renal function

Non-proliferative process (epithelial)

18

What are the complications of nephrotic syndrome? Explain each one

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

19

In which two methods might glomerulonephritis be classified?

Aetiology based
Histologically

20

What are the causes of glomerulonephritis?

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

21

By which methods can glomerulonephritis be histologically classified?

Biopsy
Microscopy
Immunofluroscence
Electron microscopy

22

What are the histological classifications of GN?

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)

23

When would you find crescentic injury?

Vasculitic GN (rapidly progressing)

24

What are the two methods of glomerulonephritis treatment?

Immunosuppressive and non immunosuppressive

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)

Decks in Year 2 Class (72):