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Lecture 13 - Glomerular Diseases (clinical) Flashcards

1
Q

What are glomerular diseases?

A

Inflammatory disorders of the kidney

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2
Q

What are glomerular diseases classified on? What investigation is necessary to differentiate them?

A

Morphology

Biopsy

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3
Q

What are the typical clinical features of a glomerulonephritis?

A

Haematuria
Proteinuria
Hypertension
Renal insufficiency

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4
Q

What are the types of haematuria?

A

Macroscopic/franks vs microscopic

Persistent vs transient

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5
Q

Define microscopic haematuria

A

5+ RBC per high power field

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6
Q

Is haematuria more typical of nephrotic or nephritic syndrome?

A

Nephritic

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7
Q

What can be the sources of blood in haematuria?

A

Kidney, ureter, bladder, urethra, prostate

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8
Q

What kind of haematuria do you tend to see in glomerulonephritis?

A

Persistent macroscopic haematuria (microscopy shoes dysmorphic RBCs)

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9
Q

Where abouts is the problem if you have proteinuria?

A

Glomerulus/tubules

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10
Q

How can you measure proteinuria?

A

Urine protein creatinine ratio

24 hour urine collection

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11
Q

What kind of proteinuria do you tend to see in glomerulonephritis?

A

Persistent proteinuria of more than 1g/mmol creatinine

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12
Q

Is hypertension more typical of nephritic or nephrotic syndrome?

A

Nephritic

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13
Q

What features are typical of nephritic syndrome?

A 
Haematuria
Mild/moderate proteinuria
Hypertension 
Oliguria
Red cell casts in the urine
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14
Q

What features are typical of nephrotic syndrome?

A

Oedema
Proteinuria >3.5g/day
Hypoalbuminaemia (<30g/L)
Hyperlipidaemia

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15
Q

What will you see on urinalysis of someone with nephrotic syndrome?

A

Proteinuria (protein ++++)

Frothy appearance

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16
Q

Why are individuals with nephrotic syndrome predisposed to thrombosis?

A

Loss of antithrombin III, proteins C and S and associated rise in fibrinogen levels

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17
Q

What are differential diagnoses for nephrotic syndrome and how could you differentiate them from nephrotic syndrome?

A

Congestive heart failure (JVP raised, normal albumin, minimal proteinuria)

Hepatic disease (abnormal LFTs, no proteinuria)

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18
Q

What are the aetiologies of glomerulonephritis?

A

Autoimmune
Infection
Malignancy
Drugs

NB same diseases can be caused by different things

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19
Q

What are the two subtypes of GNs?

A

Proliferative

Non-proliferative

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20
Q

What is a proliferative GN?

A

One in which there are excessive numbers of cells in glomeruli, incl infiltrating leucocytes

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21
Q

What is a non-proliferative GN?

A

Glomeruli appear normal or have areas of scarring

Normal number of cells

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22
Q

What is meant by a diffuse GN?

A

> 50% glomeruli affected

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23
Q

What is meant by a focal GN?

A

<50% of glomeruli affected

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24
Q

What is meant by a global GN?

A

All glomerulus affected

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25
What is meant by a segmental GN?
Part of glomerulus affected
26
What GNs cause a nephrotic syndrome?
Minimal change disease | Membranous nephropathy
27
What GNs cause a nephritic state?
ANCA associated GN Post-infectious GN Crescentic GN Diffuse proliferative GN
28
What GN largely just causes proteinuria and urinary sediment abnormalities?
IgA nephropathy
29
What GNs can cause nephrotic/nephritic state?
FSGS | Mesangioproliferative GN
30
List 4 of the proliferative GNs
Diffuse proliferative - post-infective nephritis Focal proliferative - mesangial IgA Focal necrotizing (crescentic) nephritis Membrano-proliferative nephritis
31
What nodules do you see in post-infectious GN?
Kimmersteil-Wilson nodules | May also see IgA deposits
32
What is the natural history of post-strep GN?
Follows 10-21d post throat/skin infection
33
What organism most commonly causes post-strep GN?
Lancefield group A strep (usually strep pyogenes)
34
What alleles genetically predispose someone to getting post-strep GN?
HLA-DR, -DP
35
What causes post-strep GN?
Immune complexes (IgG, IgM, C3) deposition in the glomeruli
36
Who is most affected by post-strep GN?
Young children usually
37
What are the clinical features of post-strep GN?
``` Headache, malaise Haematuria Proteinuria HTN Low C3 Raised ASO titre 1-2w post URTI (more nephritic state, e.g. red cell casts etc) ```
38
How is post-strep GN treated?
Vasodilator drugs, e.g. amlodipine for HTN | Loop diuretics, e.g. frusemide if any oedema
39
What is the commonest GN worldwide?
IgA nephropathy
40
What characterises IgA nephropathy?
IgA deposition in the mesangium + mesangial proliferation
41
Who most commonly gets IgA nephropathy?
20-30 yo males
42
What % of cases of IgA nephropathy progress to ESRD?
40%
43
How can IgA nephropathy present?
Microscopic haematuria (can be silent for a while) Microscopic haematuria + proteinuria Nephrotic syndrome IgA crescentic GN
44
What is IgA nephropathy AKA?
Berger's disease
45
How does IgA nephropathy classically present?
Macroscopic haematuria in young people following an URTI | typically nephritic syndrome!
46
What conditions are associated with IgA nephropathy?
Alcoholic cirrhosis Coeliac disease/dermatitis herpetiformis HSP
47
What do you see on histology in IgA nephropathy?
Mesengial hypercellularity | Positive immunofluorescence for IgA + C3
48
What is a marker of good prognosis in IgA nephropathy?
Frank haematuria
49
What is a marker of poor prognosis in IgA nephropathy?
``` Male grnder Proteinuria (esp >2g/day) HTN Smoking Hyperlipidaemia ACE genotype DD ```
50
What are the types of crescentic GN?
ANCA associated: microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis Anti-GBM - e.g. anti-GBM nephritis or Goodpasture's syndrome Others - IgA vasculitis, post-infection GN, SLE
51
What is goodpastures syndrome?
A rare condition associated with pulmonary haemorrhage and rapidly progressive GN
52
What causes goodpastures syndrome?
Anti-glomerular basement membrane antibodies against type IV collagen
53
What HLA allele is associated with goodpastures syndrome?
HLA DR2
54
What factors in goodpastures syndrome increase the likelihood of pulmonary haemorrhage?
``` Smoking LRTI Pulmonary oedema Inhalation of hydrocarbons Young male ```
55
How do you investigate suspected goodpasture syndrome?
Renal biopsy (linear IgG deposits along the basement membrane)
56
What is involved in the management of goodpastures syndrome?
Plasmapheresis Steroids Cyclophosphamide
57
What causes anti-GBM disease?
Circulating anti-GBM antibodies
58
How can anti-GBM present?
Nephritis - anti-GBM glomerulonephritis | Nephritis + lung haemorrhage (Goodpastures)
59
How is anti-GBM disease treated?
Aggressive immunosuppression - steroids, plasma exchange, cyclophosphamide
60
How is crescentic GN managed?
Corticosteroids, plasma exchange, cyclophosphamide, B cell therapy (e.g. rituximab), complement inhibitors
61
What does 10-20% of anti-GBM disease progress to?
Crescentic GN
62
How do proliferative GNs present?
Nephritic syndrome
63
What are the main non-proliferative GNs?
Minimal change disease Focal and segmental GN Membranous nephropathy
64
How is nephrotic syndrome managed?
Treat oedema --> fluid + salt restriction, loop diuretics HTN: RAAS blockade Reduce risk thrombosis: heparin/warfarin Reduce risk of infection e.g. pneumococcal vaccine Treat dyslipidaemia, e.g. with statins
65
Who is minimal change disease the most common GN in?
Children
66
How does minimal change disease tend to present?
Sudden onset oedema (nephrotic syndrome)
67
How is minimal change disease treated?
Steroids (prednisolone 1mg/kg for up to 16w, taper over 6m once remission achieved)
68
What fraction of pts with minimal change disease relapse?
2/3rd
69
If someone has a relapse of minimal change disease how is this managed?
``` Cyclophosphamide Cyclosporin Tacrolimus Mycophenolate mofetil Rituximab ```
70
What is the prognosis of minimal change disease?
1/3 - just one episode 1/3 - infrequent episodes 1/3 - frequent episodes which stop before adulthood
71
Does minimal change disease present as a nephrotic or nephritic syndrome?
Nephrotic
72
What are the aetiologies for minimal change disease?
Usually idiopathic Drugs: NSAIDs, rifampicin Hodgkin's lymphoma, thymoma IM
73
What is the pathophysiology of minimal change disease?
T-cell and cytokine mediated damage to the glomerular basement membrane --> polyanion loss Resultant reduction of electrostatic change --> increased glomerular permeability to albumin
74
What are the features of minimal change syndrome?
Nephrotic syndrome | Highly selective proteinuria (only medium sized proteins, e.g. albumin + transferrin)
75
What do you see on renal biopsy in minimal change disease?
Normal glomeruli on light microscopy | Electron microscopy shows fusion of podocytes + effacement of foot processes
76
What % of minimal change disease is steroid responsive?
80% | Cyclophosphamide next step for steroid resistant cases
77
What is focal and segmental GN?
A syndrome with multiple causes
78
Does focal and segmental GN present with a nephritic or nephrotic syndrome?
Nephrotic
79
What do you see on histology in focal and segmental GN?
Focal + segmental sclerosis with distinctive patterns, e.g. tip lesion, collapsing, cellular etc.
80
Can focal and segmental GN be treated with steroids?
No - usually v. steroid resistant
81
What is the prognosis of focal and segmental GN?
High chance of progression to ESRD
82
How is focal and segmental GN managed?
General measures for nephrotic syndrome, e.g. treat oedema, HTN etc. Trial steroids, even if partial remission Alt options: cyclophosphamide, cyclosporin, rituximab
83
What is focal and segmental GN aka?
Focal segmental glomerulosclerosis
84
Who does FSGS normally present in?
Young adults
85
What are causes of FSGS?
``` Idiopathic 2 to other renal pathology, e.g. IgA nepropathy, reflux nephropathy HIV Heroin Alport's syndrome Sickle-cell ```
86
What is the recurrence rate of FSGS like post-transplant?
V. high
87
What do you see on renal biopsy in FSGS?
Focal + segmental sclerosis + hyalinosis on light microscopy | Effacement of foot processes on electron microscopy
88
What is the commonest cause of nephrotic syndrome in adults?
Membranous nephropathy (usually idiopathic)
89
What antibody is present in 70% cases of membranous nephropathy?
Anti-phospholipase A2 receptor antibody
90
What are secondary causes of membranous nephropathy?
``` Malignancies - lung cancer, lymphoma, leukaemia SLE RA Infections - hep B, malaria, syphillis Drugs - NSAIDs, gold, penicillamine ```
91
What other marker is screened for in membranous nephropathy (apart from PLA2R)?
Thrombospondin type 1 domain containing 7A
92
What can you see on electromicroscopy in membranous nephropathy?
Basement membrane is thickened with subepithelial electron dense deposits - creates a spike and dome appearance
93
How is membranous nephropathy managed?
ACEi/ARB General measures for at least 6m Immunosupression if severe/progressive disease Corticosteroids tend to be used in combo with another agent, e.g. cyclophosphamide Anticoagulation for high risk pts
94
What is the prognosis of membranous nephropathy?
1/3rd: spontaneous remission 1/3rd remain proteinuric 1/3rd develop ESRD
95
What is membranoproliferative GN AKA?
Mesangiocapillary GN
96
How can membranoproliferative GN present?
Nephrotic syndrome, haematuria or proteinuria
97
What is the prognosis of membranoproliferative GN?
Poor
98
What the different types of membranoproliferative GN?
Type 1 Type 2 Type 3
99
What is the most common type of membranoproliferative GN?
Type 1 (90%)
100
What are the causes of type 1 membranoproliferative GN?
Cryoglobinaemia | Hepatitis C
101
What do you see on electromicroscopy on membranoproliferative GN?
Subendothelial and mesangium immune desposits of electron dense material --> tram track appearance
102
What is type 2 membranoproliferative GN?
Dense deposit disease Caused by persistent activation of alternative complement pathway Causes - partial lipodystrophy, factor H deficiency
103
What blood result abnormality do you see in patients with type 2 membranoproliferative GN?
Low circulating levels of C3
104
What do you see on electron microscopy in type 2 membranoproliferative GN?
Intramembranous immune complex deposits with dense deposits
105
What are causes of type 3 membranoproliferative GN?
Hep B and C
106
How can membranoproliferative GN be treated?
Steroids may be effective
107
What is rapidly progressive GN?
Term used to describe a rapid loss of renal function assoc. w formation of epithelial crescents in the majority of glomeruli
108
What are causes of rapidly progressive GN?
Goodpastures syndrome Wegner's granulomatosis SLE, microscopic polyarteritis
109
What are features of rapidly progressive GN?
Nephritic syndrome + features specific to underlying cause, e.g. vasculitis rash and sinusitis with Wegners

Renal/Urology (29 decks)

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