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Stage 3 > Nephrology: Nephritis > Flashcards

Nephrology: Nephritis Flashcards

1
Q

What is poststreptococcal glomerulonephritis?

A

A type of glomerular nephritis that occurs after a streptococcal throat or skin infection

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2
Q

How soon after a streptococcal throat infection can poststreptococcal glomerulonephritis occur?

A

1-2 weeks

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3
Q

How soon after a streptococcal skin infection can poststreptococcal glomerulonephritis occur?

A

2-6 weeks

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4
Q

What is poststreptococcal glomerulonephritis caused by?

A

Certain strains of group A beta-haemolytic streptococci

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5
Q

How does poststreptococcal glomerulonephritis occur?

A

Immune complex deposition, neutrophil infiltration and complement activation in the glomerulus cause inflammation and/or proliferation

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6
Q

How do patients with poststreptococcal glomerulonephritis typically present?

A

Typical nephritic syndrome presentation - Sudden onset:
1) Haematuria
2) Oliguria
3) Hypertension
4) Oedema (normally periorbital due to salt retention in the loose skin)

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7
Q

What is a typical nephritic syndrome presentation?

A

Sudden onset:
1) Haematuria
2) Oliguria
3) Hypertension
4) Oedema (normally periorbital due to salt retention in the loose skin)

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8
Q

What are differentials/conditions that can cause a nephritic syndrome picture?

A

SHARP AIM
1) SLE
2) Henoch-Schönlein purpura
3) Anti glomerular basement membrane (GBM) disease (Goodpasture’s)
4) Rapidly progressive glomerulonephritis
5) Post-streptococcal glomerulonephritis
6) Alport’s syndrome
7) IgA nephropathy
8) Membranoproliferative glomerulonephritis

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9
Q

What is the first line investigation in patients presenting with nephritic syndrome e.g. poststreptococcal glomerulonephritis ?

A

1) Urinalysis
2) Urine microscopy, culture and sensitivities (MC&S)

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10
Q

What are typical findings in urinalysis in nephritic syndrome e.g. poststreptococcal glomerulonephritis?

A

Positive for protein and/or blood

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11
Q

What are typical findings in urine MC&S in nephritic syndrome e.g. poststreptococcal glomerulonephritis?

A

1) Presence of RBCs - normally dysmorphic, which suggests bleeding from the glomerulus
2) Presence of WBCs - neutrophil infiltration is one of the mechanisms of damage in nephritic syndrome) and associated casts

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12
Q

Which blood tests should be done in nephritic syndrome e.g. poststreptococcal glomerulonephritis and why?

A

1) FBC - to look for raised white cells, suggestive of an infective process
2) U&Es - can suggest AKI

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13
Q

Which tests can be done in nephritic syndrome e.g. poststreptococcal glomerulonephritis to help delineate an autoimmune process?

A

1) Immunoglobulins
2) Complement (low C3 levels normally found)
3) Autoantibodies e.g. raised anti-streptolysin titre, raised DNAse B titre

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14
Q

Which additional test is indicated in patients with nephritic syndrome e.g. poststreptococcal glomerulonephritis who have a fever?

A

Blood cultures

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15
Q

What is the gold standard method for diagnosis of nephritic syndrome e.g. poststreptococcal glomerulonephritis?

A

Renal biopsy

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16
Q

Which test is rarely helpful in nephritic syndrome e.g. poststreptococcal glomerulonephritis?

A

Imaging

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17
Q

How do you manage poststreptococcal glomerulonephritis?

A

Supportive measures

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18
Q

What are potential complications of poststreptococcal glomerulonephritis?

A

1) CKD
2) End stage renal disease

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19
Q

What is the most common cause of poststreptococcal glomerulonephritis?

A

Streptococcus pyogenes

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20
Q

What is an example of a streptococcal infection that can cause poststreptococcal glomerulonephritis?

A

Scarlet fever due to Group A beta-haemolytic streptococcus, most commonly streptococcus pyogenes

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21
Q

What is the most common cause of intrinsic AKI?

A

Acute tubular necrosis (ATN)

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22
Q

What is acute tubular necrosis?

A

Damage to the tubular epithelial cells within the renal tubules of the kidney either due to ischaemia or direct toxicity - ischaemic damage or direct toxicity to the tubular epithelial cells

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23
Q

How does acute tubular necrosis present?

A

AKI - oliguria, uraemia, electrolyte imbalance (feeling generally unwell)

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24
Q

What are the two types of causes of acute tubular necrosis?

A

Ischaemic (due to hypoperfusion) and nephrotoxic

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25
Q

What are ischaemic causes of acute tubular necrosis?

A

1) Hypotension
2) Shock - haemorrhage, cardiogenic, septic (sepsis is a common cause of hypoperfusion and ischaemia in the kidney)
3) Direct vascular injury - trauma, surgery

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26
Q

What are nephrotoxic causes of acute tubular necrosis?

A

Drugs or contrast or myoglobinuria in rhabdomyolysis

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27
Q

Which drugs can cause nephrotoxic acute tubular necrosis?

A

1) Aminoglycoside antibiotics - gentamicin
2) Antifungal drugs - amphotericin
3) Chemotherapy agents - cisplatin
4) NSAIDs
5) ACEi
6) ARB - candesartan
7) Statins

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28
Q

What are management options for acute tubular necrosis?

A

1) Correction of underlying cause e.g. fluid resuscitation
2) Removal of nephrotoxins
3) May require haemofiltration or haemodialysis

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29
Q

What investigation do you do to diagnosis acute tubular necrosis?

A

Urinalysis

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30
Q

What is the pathognomonic finding of acute tubular necrosis on urinalysis?

A

Muddy brown casts

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31
Q

What is glomerulonephritis?

A

Inflammation of the glomerulus and nephron

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32
Q

What are you likely to see in urinalysis in glomerulonephritis or small-vessel vasculitis?

A

Red-cell casts

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33
Q

What is acute pyelonephritis?

A

Bacterial infection and inflammation of the kidneys

34
Q

What might you see in urinalysis in acute pyelonephritis or acute interstitial nephritis?

A

White blood cell casts (in acute pyelonephritis culture may yield the causative bacteria)

35
Q

What is acute (tubulo)interstitial nephritis thought to be caused by?

A

An interstitial hypersensitivity reaction

36
Q

What would blood results show in acute tubular necrosis?

A

Raised creatinine

37
Q

What is acute (tubulo)interstitial nephritis

A

Primary injury to renal tubules and interstitium, resulting in decreased renal function

38
Q

How does acute (tubulo)interstitial nephritis present?

A

Sudden onset AKI (usually within days of exposure to causative drug)

39
Q

What are causes of acute (tubulo)interstitial nephritis?

A

Drugs, infections, systemic autoimmune disease

40
Q

What is the classic triad in the presentation of drug-induced acute (tubulo)interstitial nephritis ?

A

Fever + rash + eosinophilia

41
Q

What is the most aggressive type of glomerulonephritis?

A

Rapidly progressive glomerulonephritis (RPGN)

42
Q

What are the features of rapidly progressive glomerulonephritis (RPGN)?

A

1) Nephritic syndrome
2) Rapid decline in renal function
3) Evidence of pulmonary and renal involvement

43
Q

Which conditions are part of rapidly progressive glomerulonephritis (RPGN)?

A

1) Goodpasture’s syndrome (anti-GBM disease)
2) Immune complex deposition e.g. SLE, granulomatosis with polyangiitis (ANCA)
3) Pauci-immune vasculitides

44
Q

What are symptoms of early hypertensive nephropathy?

A

1) Mild albuminuria
2) Reduced eGFR

45
Q

What nephrological condition does chronic, poorly controlled (malignant) hypertension cause?

A

Hypertensive arteriolar nephrosclerosis (late stage) - progressive renal impairment

46
Q

What are the features of hypertensive arteriolar nephrosclerosis (late stage)/malignant hypertension?

A

Progressive renal impairment
1) Anorexia
2) Vomiting
3) Pruritus
4) Confusion
5) Weight loss
6) Dysgeusia (taste disorder

47
Q

What is diabetic nephropathy?

A

Glomerular sclerosis and fibrosis caused by the metabolic and haemodynamic changes of diabetes

48
Q

How does diabetic nephropathy present?

A

Slowly progressive albuminuria with worsening hypertension and renal insufficiency

49
Q

Which antibodies are involved in Goodpasture’s/anti-GBM disease?

A

IgG against type IV collagen (found in GBM and lungs)
Antibodies to the non collagenous domain (NC1) of the alpha-3 chain of collagen type IV (anti-glomerular basement membrane)

50
Q

Where are the antibodies directed in anti-GBM disease?

A

Against antigens that are found on the glomerular basement membrane in the kidneys and lung alveoli

51
Q

How do you treat anti-GBM disease?

A

1) Plasmapheresis - to remove pathogenic circulating antibodies
2) Immunosuppression with high dose oral prednisolone or oral cyclophosphamide - to stop further production of antibodies (+ steroids)
3) Dialysis - if present with severe AKI (poor prognosis)
4) Renal transplantation - if end stage renal disease - optimal conditions for transplant achieved when anti-GBM antibodies are undetectable in the serum for 12 months and the disease has been in remission for at least 6 months without the use of cytotoxic agents

52
Q

What are indications for dialysis?

A

AEIOU
1) Acidosis - severe metabolic acidosis pH < 7.2
2) Electrolyte imbalances - persistent hyperkalaemia > 7
3) Intoxication - poisoning
4) Oedema - pulmonary oedema refractory to treatment
5) Uraemia - presents with either uraemic pericarditis or uraemic encephalopathy

53
Q

What is the typical histological finding in anti-GBM disease?

A

Crescent formation and linear deposition of antibodies along the glomerular basement membrane

54
Q

How does anti-GBM disease present?

A

Haemoptysis (pulmonary haemorrhage), SOB and haematuria (rapidly progressive crescentic GN)- mostly in men

55
Q

What do you see in PSGN when renal biopsy tissue is analysed under immunofluorescence?

A

Subepithelial humps in the glomeruli

56
Q

What is seen on renal biopsy in Alport syndrome?

A

Longitudinal splitting of the lamina densa causing a “basket-weave” appearance

57
Q

What is IgA nephropathy?

A

A type of glomerulonephritis characterised by IgA deposition in the mesangium

58
Q

Which is the most common immunoglobulin in mucosal secretions?

A

IgA

59
Q

What causes IgA nephropathy?

A

1) In certain genetically predisposed people, there is an increased synthesis of a particular type of IgA secondary to resp or gastro infection
2) These types of IgA form immune complexes that are more easily lodged in the mesangium of the glomerulus causing proliferation
3) This + activation of the alternative complement pathway causes glomerular injury

60
Q

How does IgA nephropathy present?

A

1) Recurrent gross or microscopic haematuria 12-72h after an URTI
2) Mild proteinuria
3) Hypertension

61
Q

What are potential complications of IgA nephropathy?

A

1) Rare cases may present with rapidly progressive GN where they rapidly progressive to acute renal failure
2) Slow progression to chronic renal failure occurs in 15-40% of patients

62
Q

What conditions can cause a nephritic picture?

A

SHARP AIM
1) SLE
2) Henoch-Schönlein purpura (HSP)
3) Anti-GBM disease
4) Rapidly progressive GN
5) Post-streptococcal GN
6) Alport’s syndrome
7) IgA nephropathy (Berger’s disease)
8) Membranoproliferative GN

63
Q

What are the first line investigations for IgA nephropathy?

A

Urinalysis and urine MC&S

64
Q

What would urinalysis show in IgA nephropathy?

A

Positive for blood ± protein (only 5% of patients will present with nephrotic range proteinuria (>3-3.5g/24hr))

65
Q

What would urine MC&S show in IgA nephropathy?

A

1) Presence of RBCs - normally dysmorphic which suggests bleeding from the glomerulus
2) Presence of WBCs - neutrophil infiltration is one of the mechanisms of damage in nephritic syndrome
3) Associated casts

66
Q

What is the gold standard method for diagnosis of IgA nephropathy?

A

Renal biopsy

67
Q

What would renal biopsy with immunofluorescence show in IgA nephropathy?

A

IgA deposited in a granular pattern in the mesangium (glomerulus)

68
Q

How do you differentiate between IgA nephropathy and PSGN?

A

1) IgA nephropathy occurs 1-2 days post-infection (vs. 1-3 weeks post-infection in PSGN)
2) Renal biopsy in IgA nephropathy shows IgA immune complex deposits (vs. IgG immune complex deposits in PSGN)

69
Q

What blood tests would you do in IgA nephropathy?

A

1) FBC - to look for raised WBCs, suggestive of an infective process
2) U&Es - to look for raised urea and creatinine suggesting AKI (only occurs in < 5% of patients)
3) Blood cultures - in patients with fever

70
Q

How do you manage IgA nephropathy?

A

1) Conservative - monitoring and optimising fluid balance
2) Optimising BP
3) ACEi/ARB - to reduce proteinuria and protect renal function
4) Corticosteroids - can also help to decrease proteinuria

71
Q

What is the other name for IgA nephropathy?

A

Berger’s disease

72
Q

How does nephritic syndrome present?

A

1) Haematuria
2) Non-nephrotic range proteinuria (+/++ on urine dipstick or >3-3.5g/24hr)
3) ± hypertension (more likely in nephritis than nephrotic syndrome)

73
Q

Which nephritis syndrome presents with nephrotic-range proteinuria?

A

Membranoproliferative (mesangio-capillary) glomerulonephritis

74
Q

Which conditions present with a pure nephritic syndrome?

A

1) PSGN
2) IgA nephropathy
3) Infective endocarditis
4) Anti-GBM disease
5) Vasculitis

75
Q

What is nephrotic range proteinuria?

A

> 3-3.5g/24hr OR protein +++ urine dipstick

76
Q

What is Alport syndrome?

A

Defect in type IV collagen

77
Q

What are the clinical features of Alport syndrome?

A

1) Haematuria (nephritic syndrome)
2) Proteinuria
3) Progressive renal failure
4) Sensorineural deafness
5) Lens deformities

78
Q

How is Alport syndrome managed?

A

1) ACEi - should be given to all patients with proteinuria bc helps to slow the progression of the disease
2) Patients with ultimately require RRT - haemodialysis or kidney transplant

79
Q

Which medication is used in the management of glomerulonephritides?

A

Corticosteroids

80
Q

Which patients are most likely to present with IgA nephropathy (recurrent episodes of macroscopic haemturia)?

A

Young males

81
Q

What would you see on renal biopsy in advanced sclerosing lupus nephritis?

A

Global sclerosis of glomeruli

Stage 3 (61 decks)

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