Glomerular Disease (Clinical) Flashcards

1
Q

What is glomerulonephritis?

A

Acute inflammation of the kidney, typically caused by an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are glomerular diseases?

A

Immune-mediated disorders that affect the glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are glomerular diseases classified by?

A

Based on kidney biopsy findings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 2 different classifications of glomerular diseases?

A
  • Proliferative
    • IgA nephropathy
    • Post infectious glomerulonephritis
    • Crescentic glomerulonephritis
    • Anti-GBM disease
  • Non-proliferative
    • Minimal change disease
    • Focal and segmental glomerulosclerosis
    • Membranous nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are examples of proliferative glomerular diseases?

A
  • IgA nephropathy
  • Post infectious glomerulonephritis
  • Crescentic glomerulonephritis
  • Anti-GBM disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some examples of non-proliferative glomerular diseases?

A
  • Minimal change disease
  • Focal and segmental glomerulosclerosis
  • Membranous nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 kinds of glomerulonephritis syndromes?

A

Nephritic syndrome

Nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some features of glomerulonephritis?

A
  • Haematuria (non visible or visible)
  • Proteinuria (low grade or nephrotic)
  • Hypertension
  • Renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is observed if glomerulonephritis is in a nephritic state?

A
  • Active urine sediment
    • Haematuria
    • Dysmorphic RBCs
    • Cellular casts
  • Hypertension
  • Renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is observed if glomerulonephritis is in a nephrotic state?

A
  • Body passes too much protein in urine
  • Oedema
  • Nephrotic range proteinuria
    • >3.5g/day or 350mg/mmol creatinine
  • Hypoalbuminaemia
    • Serum albumin <35g/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the range of proteinuria required to be considered a nephrotic syndrome?

A
  • >3.5g/day or 350mg/mmol creatinine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between nephritic and nephrotic syndromes?

A

Difference between nephritic and nephrotic is that nephrotic syndrome involves the loss of a lot of protein whereas nephritic syndrome involves the loss of a lot of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is proliferative glomerulonephritis defined as?

A

Excessive numnbers of cells in glomeruli, these include infiltrating leucocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is non-proliferative glomerulonephritis defined as?

A

Glomeruli look normal or have areas of scarring

They have normal numbers of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the pathological descriptions of glomerulonephritis depending on how much of the glomeruli is affected?

A
  • Diffuse
    • >50% of glomeruli affected
  • Focal
    • <50% of glomeruli affected
  • Global
    • All of the glomerulus affected
  • Segmental
    • Part of the glomerulus affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the term used to describe >50% of the glomeruli is affected?

A

Diffuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the term used to describe <50% of the glomeruli is affected?

A

Focal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the term used to describe all of the glomeruli is affected?

A

Global

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the term used to describe part of the glomeruli is affected?

A

Segmental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Are non-proliferative diseases normally nephrotic or nephritic?

A

Nephrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Are proliferative diseases normally nephrotic or nephritic?

A

Nephritic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the commonest cause of glomerulonephritis?

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is IgA nephropathy characterised by?

A

IgA deposition in th emesangium and mesangial proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Who does IgA nephropathy most commonly occur in?

A

Most commonly occurs in 2nd and 3rd decade of life with males more commonly affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Does IgA nephropathy affect more men or woman?

A

Men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the presentation of IgA nephropathy?

A
  • Microscopic haematuria
  • Microscopic haematuria and proteinuria
  • Nephrotic syndrome
  • IgA crescentic glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What investigations are done for IgA nephropathy?

A
  • Urine dip
  • Blood pressure
  • Ultrasound scan
  • Renal biopsy
  • eGFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the treatment for IgA nephropathy?

A
  • Dialysis
  • Renal transplant
29
Q

What is post infectious glomerulonephritis most commonly caused by?

A

Most commonly caused by Lancefield group A streptococci infection after infection typically of throat or skin

30
Q

Is there a genetic predisposition to post infectious glomerulonephritis?

A

Yes

HLA-DR, -DP

31
Q

What is the presentation of post infectious glomerulonephritis?

A
  • Malaise
  • Dark urine
  • Puffy face
  • No rashes or oedema
  • Sore throat previously
32
Q

What investigations are done for post infectious glomerulonephritis?

A
  • Bloods
  • Urine dip
33
Q

What is the treatment of post infectious glomerulonephritis?

A
  • Antibiotics for infection
  • Loop diuretics such as frusemide for oedema
  • Anti-hypertensives such as vasodilator drugs
34
Q

What are the different kinds of crescentic glomeronephritis?

A

Anti-neutrophil cytoplasmic antobody (ANCA) associated

Anti-glomerular basement membrane (GBM)

Others (IgA vasculitis, post infection glomerulonephritis, lupus nephritis)

35
Q

What is lupus nephritis caused by?

A
36
Q

What is the presentation of crescentic glomerulonephritis?

A
  • Fatigue
  • Weight loss
  • Rash
  • Bilateral basal crepitations
37
Q

What is crescentic glomerulonephritis characterised by?

A

Characterised by the presence of extensive glomerular crescents (usually greater than 50%) as the principal histologic finding

38
Q

What investigations are done for crescentic nephritis?

A
  • Urine dipstick
    • High protein and high blood
  • Bloods
    • High serum creatinine
  • Renal biopsy
39
Q

What is observed in urine dipsticks for crescentic glomerulonephritis?

A

High protein and high blood

40
Q

What is observed in the bloods for crescentic glomerulonephritis?

A

High serum creatinine

41
Q

What is anti-GBM disease?

A

Rare disease caused by circulating anti-GBM, is a type of crescentic glomerulonephritis

42
Q

What does anti-GBM disease present as?

A
  • Nephritis (anti-GMB glomerulonephritis)
  • Nephritis and lung haemorrhage
43
Q

In what age groups is anti-GBM disease most common?

A

Peaks in 3rd and 6th/7th decade of life

44
Q

How is anti-GBM disease diagnosed?

A

Diagnosed by demonstrating anti-GBM antibodies in serum and kidney

45
Q

What is the treatment for anti-GBM disease?

A
  • Aggressive immunosuppression
  • Steroids
  • Plasma exchange
  • Cyclophosphamide
46
Q

Do proliferative glomerulonephritis’s present with nephrotic or nephritic state?

A

Presents with nephritic stage:

  • Haematuria and variable proteinuria and hypertension with or without renal impairment
47
Q

Why is early diagnosis important in proliferative glomerulonephritis’s?

A

Early diagnosis necessary to save nephrons:

  • Clinical suspicion, immunological screen and renal biopsy
48
Q

What are the pathological patterns of non-proliferative glomerulonephritis?

A

Focal and segmental glomerulonephritis

49
Q

What is the management for non-proliferative glomerulonephritis?

A
  • General measures
    • Treat oedema
      • Salt and fluid restriction and loop diuretics
    • Hypertension
      • RAAS blockade
    • Reduce risk of thrombosis
      • Heparin or warfarin
    • Treat dyslipidaemia
      • Statins
  • Specific therapy
    • Towards cause of non-proliferative glomerulonephritis
50
Q

What is the commonest form of non-proliferative glomerulonephritis in children?

A

Minimal change disease

51
Q

What is the presentation of minimal change disease?

A

Sudden onset of oedema

52
Q

How often does relapse occur in minimal change disease?

A

2/3 of patients

53
Q

What is the treatment for minimal change disease?

A
  • Prednisolone
    • 1mg/kg for up to 16 weeks
    • Once remission achieved, slow taper over 6 months
  • Initial relapse treated with further steroid course
  • Subsequent relapses treated with
    • Cyclophosphamide
    • Cyclosporin
    • Tacrolimus
    • Mycophenolate mofetil
    • Rituximab
54
Q

What is the prognosis of minimal change diease?

A
  • Despite relapsing behaviour, prognosis is favourable
  • Risk of end stage kidney disease is low
  • Steroids toxicity as multiple exposure
55
Q

What is focal and segmental glomerulosclerosis (FSGS)?

A

Disease in which scar tissue develops on the parts of the kidneys that filter waste from the blood (glomeruli)

Is not a single disease, rather a syndrome with multiple causes

56
Q

What pathological pattern does FSGS display?

A

Pathology reveals focal and segmental sclerosis with distinctive patterns, such as:

  • Tip lesion, collapsing, cellular, perihilar and not other specified
57
Q

What does FSGS stand for?

A

Focal and segmental glomerulosclerosis

58
Q

Wnat is the prognosis of FSGS?

A

High change of progression to end stage kidney disease

59
Q

What is the treatment for FSGS?

A
  • General measures as previously described
  • Trail of steroids
  • Alternative options
    • Cyclosporin
    • Cyclophosphamide
    • Rituximab
60
Q

What are the different kinds of FSGS?

A

Primary or secondary

61
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

62
Q

What are some serological markers for membranous nephropathy?

A
  • Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases
  • Thrombospondin type 1 domain containing 7A
63
Q

What are some secondary causes of membranous nephropathy?

A
  • Malignancies
  • SLE
  • Rheumatoid arthritis
  • Drugs
    • NSAIDs, gold, penicillamine
64
Q

What is the treatment of membranous nephropathy?

A
  • General measures for at least 6 months
  • Immunosuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function
  • Cyclophosphamide and steroids for 6 months
  • Tacrolimus
  • Rituximab
65
Q

What is the prognosis of membranous nephropathy?

A
  • Resolves spontaneously in 1/3
  • Prognosis good in treated patients whose proteinuria resolves
  • About 25% are on dialysis in 10 years
  • Can recur in renal transplants
66
Q

Does non-proliferative glomerulonephritis present with nephrotic or nephritic syndrome?

A

Nephrotic syndrome

67
Q

What does precise diagnoisis of the kind of glomerular disease depend on?

A

Renal biopsy which can influence management

68
Q

What does the prognosis of glomerular disease depend on?

A

Type of glomerulonephritis and the response to treatment