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Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis

A

Damage to glomerulus including glomerular basement membrane and glomerular capillaries, usually caused by inflammatory changes

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2
Q

Types of glomerulonephritis

A

Memrbanous glomerulonephritis, minimal change disease, focal-segmental glomerulonephritis, IgA nephropathy, rapidly progressing glomerulonephritis, lupus nephritis, post-infectious glomerulonephritis, anti-GBM disease

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3
Q

Infectious causes of glomerulonephritis

A

Group A strep, Hep B + C, respiratory and GI infections, endocarditis, HIV

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4
Q

Systemic causes of glomerulonephritis

A

Lupus, rheumatoid arthritis, anti-GBM, microscopic polyangitis, granulomatosis polyangitis, amyloidosis

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5
Q

Drugs which can cause glomerulonephritis

A

NSAIDs, gold, anabolic steroids

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6
Q

Metabolic disorders which can cause glomerulonephritis

A

Diabetes, hypertension, thyroid disease, malignancy, Alport’s

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7
Q

Symptoms and signs of glomerulonephritis

A

Asymptomatic, haematuria, proteinuria, oedema, HTN, joint pain, rash, fever, weight loss

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8
Q

Investigations into glomerulonephritis

A

Urinalysis, urine microscopy, U&Es, FBC, metabolic profile, lipid profile, CRP, testing for specific systemic causes, US and biopsy

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9
Q

What is rapidly progressing glomerulonephritis

A

Spectrum of conditions associated with severe glomerular injury

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10
Q

Type 1 causes of RPGN

A

Anti-GBM disease

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11
Q

Type 2 causes of RPGN

A

Immune complex deposition diseases - post-strep GN, lupus nephritis, IgA nephropathy, HSP

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12
Q

Type 3 causes of RPGN

A

Pauci-immune diseases - ANCAs (pANCE or cANCA)

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13
Q

Most common causes of glomerulonephritis

A

IgA nephropathy

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14
Q

Clinical feature of IgA nephropathy

A

Haematuria, mild proteinuria, hypertension (25%), can have evidence of CKD

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15
Q

Cause of IgA nephropathy

A

In predisposed people there is the synthesis of a type of IgA secondary to a respiratory or GI infection. These IgA complexes lodge and with activation of complement pathway cause injury. IgA deposits in mesangium

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16
Q

Investigations into IgA nephropathy

A

Urinalysis, microscopy, culture and sensitivity, RBCs, WBCs and casts found.

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17
Q

How is IgA nephropathy diagnosed

A

Histologically with immunofluorescence showing IgA deposits in a granular pattern

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18
Q

GOLD standard for IgA nephropathy

A

Renal biopsy

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19
Q

Outcomes of IgA nephropathy

A

Unpredictable, 20-30% progress to ESRF in <20 years

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20
Q

Management of IgA nephropathy

A

Monitoring and optimising fluid balance, supportive treatment for complications of AKI or CKD. ACEI/ARB helps reduce proteinuria and protects renal function. Corticosteroids and sometimes immunosuppression

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21
Q

Clinical features of anti-GBM disease

A

Abrupt onset anuria, renal failure, nephritis, haemoptysis, haematesis, acute respiratory failure and pulmonary haemorrhage

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22
Q

What is Goodpasture’s syndrome

A

Pulmonary haemorrhage and RPGN

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23
Q

What is Goodpasture’s disease

A

Secondary to anti-GBM antibodies

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24
Q

Causes of anti-GBM disease

A

Autoimmune and hypersensitivity type II reaction when target kidney BM and lung alveoli

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25
Aims of therapy for anti-GBM disease
Removing circulating antibodies and immunosuppression with medication to stop further antibody production
26
Management of anti-GBM disease
Plasmaphoresis, cyclophosphamide, methylprednisolone. If there is severe AKI then may require dialysis or transplant
27
Triad of features in haemolytic uraemic syndrome
Microangiopathic haemolytic anaemia, thrombocytopenia and AKI
28
Pathophysiology behind HUS
RBCs are being destroyed and platelets are being used up. Toxin damages endothelial cells and causes thrombus formation within the arteries.
29
Four aetiologies behind HUS
Infection-induced, dysregulation of complement, drugs and miscellaneous
30
Toxin that causes HUS
Most commonly the verotoxin from E.coli (shiga toxin) or sometimes Shigella.
31
Spread of HUS
Contaminated from meat or human to human
32
Symptoms of HUS
Incubation period of 3-8 days, then vomiting, diarrhoea, cramps, oliguria, hypotension, haematuria, low grade pyrexia
33
Signs of HUS
Pale (anaemia), jaundiced (haemolysis), bruising (thrombocytopenia), abdominal tenderness
34
What does urine dipstick show in HUS
shows haematuria/proteinuria (non-nephrotic range)
35
What will investigations into HUS show
Normocytic anaemia, thrombocytopenia, potentialy raised neutrophils, raised urea and creatinine, clotting normal. E.coli culture
36
What would a blood film reveal in HUS
Reticulocytes and fragmented red cells
37
Management of HUS
Fluids for hyvolaemia, if severe dialysis is required, plasma exchange needed
38
What should not be given in HUS
Abx as it can increase the release of the toxin
39
Cause of post-infectious glomerulonephritis
Streptococcal throat infection or streptococcal skin infection - strains of group A beta-haemolytic streptococci
40
Time course for post-infectious GN
1-2 weeks after strep throat and 2-6 weeks after strep skin infection
41
Symptoms of post-infectious GN
'coca-cola' urine, sudden onset haematuria, oliguria, HTN, periorbital oedema, proteinuria
42
Typical age for post-infectious GN
<30 years old
43
Diagnosis of post-infectious GN
Infection markers raised in FBC, U&Es suggesting AKI, low C3 levels, urinalysis and MC&S
44
GOLD standard in diagnosis of post-infectious GN
Biopsy
45
Management of post-infectious GN
Supportive as usually resolves, severe cases can result in CKD, treat complications
46
Clinical featurse of minimal change disease
Proteinuria, loss of albumin and oedema. Typically well before presentation, facial swelling, can be asymptomatic
47
What is minimal change disease the most common cause of
Nephrotic syndrome in children
48
Diagnosis of minimal change disease
Urine analysis - small MW proteins and hyaline casts. Electron microscopy
49
What does electron microscopy show
Electron microscopy shows podocytes with diffuse effacement of foot processes
50
Management of minimal change disease
90% respond well to steroids (prednisolone), fluid resus, salt reduction
51
Complications of minimal change disease
Spontaneous peritonitis, thrombosis, recurrence/relapse, HTN
52
What is membranous nephropathy the most common cause of
Nephrotic syndrome in adults
53
Clinical features of membranous nephropathy
proteinuria, but not as much inflammation
54
Causes of membranous nephropathy
80% idiopathic,20% secondary and associated with SLE, infections, drugs, malignancy.
55
Pathophysiology behind membranous nephropathy
autoimmune response with antigen to podocyte foot processes - most common
56
Outcomes of membranous nephropathy
1/3 partial remission, 1/3 long term proteinuria, 1/3 develope renal failure
57
Management of membranous nephropathy
Poor responses to steroids, control BP, and if high risk can use immunosuppressants
58
What is lupus nephritis
When SLE involves the kidneys
59
Symptoms of lupus nephritis
Can be asymptomatic before presentation, or have nephritic or nephrotic syndrome
60
Diagnosis of lupud nephritis
Diagnostic test of anti-dsDNA
61
Ivestigations into lupus nephritis
Blood tests would show increased plasma urea, creatinine, and reduced GFR. Urine dipstick shows proteinuria
62
Management of lupus nephritis
High dose steroids, immunosuppression
63
What is diabetic nephropathy
Manifestation of diabetic microvascular disease involving renal arterioles and glomeruli.
64
What is the most common cause of CKD
Diabetic nephropathy
65
Feature of diabetic nephropathy
Microalbuminaemia in early stages progressing to more severe proteinuria. Chronic high levels of glucose which cause fibrosis. There focal and segmental glomerulosclerosis
66
Management of diabetic nephropathy
Regular screening, control of diabetes, blockage of RAS with ACEIs

Renal Medicine (11 decks)

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