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Renal Medicine > Glomerulonephritis > Flashcards

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
Q

Aims of therapy for anti-GBM disease

A

Removing circulating antibodies and immunosuppression with medication to stop further antibody production

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26
Q

Management of anti-GBM disease

A

Plasmaphoresis, cyclophosphamide, methylprednisolone. If there is severe AKI then may require dialysis or transplant

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27
Q

Triad of features in haemolytic uraemic syndrome

A

Microangiopathic haemolytic anaemia, thrombocytopenia and AKI

28
Q

Pathophysiology behind HUS

A

RBCs are being destroyed and platelets are being used up. Toxin damages endothelial cells and causes thrombus formation within the arteries.

29
Q

Four aetiologies behind HUS

A

Infection-induced, dysregulation of complement, drugs and miscellaneous

30
Q

Toxin that causes HUS

A

Most commonly the verotoxin from E.coli (shiga toxin) or sometimes Shigella.

31
Q

Spread of HUS

A

Contaminated from meat or human to human

32
Q

Symptoms of HUS

A

Incubation period of 3-8 days, then vomiting, diarrhoea, cramps, oliguria, hypotension, haematuria, low grade pyrexia

33
Q

Signs of HUS

A

Pale (anaemia), jaundiced (haemolysis), bruising (thrombocytopenia), abdominal tenderness

34
Q

What does urine dipstick show in HUS

A

shows haematuria/proteinuria (non-nephrotic range)

35
Q

What will investigations into HUS show

A

Normocytic anaemia, thrombocytopenia, potentialy raised neutrophils, raised urea and creatinine, clotting normal. E.coli culture

36
Q

What would a blood film reveal in HUS

A

Reticulocytes and fragmented red cells

37
Q

Management of HUS

A

Fluids for hyvolaemia, if severe dialysis is required, plasma exchange needed

38
Q

What should not be given in HUS

A

Abx as it can increase the release of the toxin

39
Q

Cause of post-infectious glomerulonephritis

A

Streptococcal throat infection or streptococcal skin infection - strains of group A beta-haemolytic streptococci

40
Q

Time course for post-infectious GN

A

1-2 weeks after strep throat and 2-6 weeks after strep skin infection

41
Q

Symptoms of post-infectious GN

A

‘coca-cola’ urine, sudden onset haematuria, oliguria, HTN, periorbital oedema, proteinuria

42
Q

Typical age for post-infectious GN

A

<30 years old

43
Q

Diagnosis of post-infectious GN

A

Infection markers raised in FBC, U&Es suggesting AKI, low C3 levels, urinalysis and MC&S

44
Q

GOLD standard in diagnosis of post-infectious GN

45
Q

Management of post-infectious GN

A

Supportive as usually resolves, severe cases can result in CKD, treat complications

46
Q

Clinical featurse of minimal change disease

A

Proteinuria, loss of albumin and oedema. Typically well before presentation, facial swelling, can be asymptomatic

47
Q

What is minimal change disease the most common cause of

A

Nephrotic syndrome in children

48
Q

Diagnosis of minimal change disease

A

Urine analysis - small MW proteins and hyaline casts. Electron microscopy

49
Q

What does electron microscopy show

A

Electron microscopy shows podocytes with diffuse effacement of foot processes

50
Q

Management of minimal change disease

A

90% respond well to steroids (prednisolone), fluid resus, salt reduction

51
Q

Complications of minimal change disease

A

Spontaneous peritonitis, thrombosis, recurrence/relapse, HTN

52
Q

What is membranous nephropathy the most common cause of

A

Nephrotic syndrome in adults

53
Q

Clinical features of membranous nephropathy

A

proteinuria, but not as much inflammation

54
Q

Causes of membranous nephropathy

A

80% idiopathic,20% secondary and associated with SLE, infections, drugs, malignancy.

55
Q

Pathophysiology behind membranous nephropathy

A

autoimmune response with antigen to podocyte foot processes - most common

56
Q

Outcomes of membranous nephropathy

A

1/3 partial remission, 1/3 long term proteinuria, 1/3 develope renal failure

57
Q

Management of membranous nephropathy

A

Poor responses to steroids, control BP, and if high risk can use immunosuppressants

58
Q

What is lupus nephritis

A

When SLE involves the kidneys

59
Q

Symptoms of lupus nephritis

A

Can be asymptomatic before presentation, or have nephritic or nephrotic syndrome

60
Q

Diagnosis of lupud nephritis

A

Diagnostic test of anti-dsDNA

61
Q

Ivestigations into lupus nephritis

A

Blood tests would show increased plasma urea, creatinine, and reduced GFR. Urine dipstick shows proteinuria

62
Q

Management of lupus nephritis

A

High dose steroids, immunosuppression

63
Q

What is diabetic nephropathy

A

Manifestation of diabetic microvascular disease involving renal arterioles and glomeruli.

64
Q

What is the most common cause of CKD

A

Diabetic nephropathy

65
Q

Feature of diabetic nephropathy

A

Microalbuminaemia in early stages progressing to more severe proteinuria. Chronic high levels of glucose which cause fibrosis. There focal and segmental glomerulosclerosis

66
Q

Management of diabetic nephropathy

A

Regular screening, control of diabetes, blockage of RAS with ACEIs

Renal Medicine (11 decks)

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