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Year 3 > Nephrotic syndrome (URO) > Flashcards

Nephrotic syndrome (URO) Flashcards

1
Q

Define nephrotic syndrome.

A

Defined as the presence of proteinuria (>3.5g/24h), hypoalbuminaemia (<30g/L) and peripheral oedema

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2
Q

What is nephrotic syndrome?

A

Collection of signs and symptoms indicating damage to the glomerular filtration barrier

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3
Q

What is nephrotic syndrome characterised by? (3)

A
  • massive proteinuria (>3.5g/24hr)
  • hypoalbuminaemia (<30g/L)
  • peripheral oedema
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4
Q

What causes proteinuria in nephrotic syndrome?

A

Glomerular damage (injury to podocytes) causes protein leakage into urine

This proteinuria –> hypoalbuminaemia and subsequent oedema due to reduced plasma oncotic pressure

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5
Q

How can nephrotic syndrome be classified?

A

Primary (idiopathic) or secondary to systemic disease

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6
Q

What are some causes/examples of nephrotic syndrome? (5)

A
  • minimal change disease (primary)
  • membranous glomerulonephritis (primary) AKA membranous nephropathy
  • focal segmental glomerulosclerosis (primary)
  • diabetic nephropathy (secondary)
  • amyloid nephropathy (secondary)
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7
Q

In which groups is minimal change disease (nephrotic syndrome) the most common cause of nephrotic syndrome?

A

Children (young <10)

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8
Q

What does minimal change disease (nephrotic syndrome) commonly present with?

A

Peri-orbital oedema

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9
Q

What diseases is minimal change disease (nephrotic syndrome) associated with? (3)

A
  • URTI
  • non-Hodgkin’s lymphoma
  • secondary to Hodgkin’s lymphoma
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10
Q

Describe the pathophysiology of minimal change disease (nephrotic syndrome).

A

Cytokine-mediated damage of podocytes (role is to prevent protein entering filtrate) - they lose their negatively-charged coat –> proteinuria

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11
Q

What will light microscopy show in minimal change disease (nephrotic syndrome)?

A

Normal light microscopy

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12
Q

Why is it called ‘minimal change disease’ (nephrotic syndrome)?

A

‘Minimal change’ refers to light microscopic findings that often reveal normal glomeruli or mild mesangial proliferation with negative immunofluorescence and no immune complex deposition

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13
Q

What will electron microscopy show in minimal change disease (nephrotic syndrome)?

A

Fusion of podocytes

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14
Q

What is the cause of minimal change disease (nephrotic syndrome)?

A

Often idiopathic

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15
Q

Describe the clinical picture of minimal change disease (nephrotic syndrome).

A

Fully nephrotic

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16
Q

What is minimal change disease (nephrotic syndrome) typically responsive to?

A

Steroids

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17
Q

How do we manage minimal change disease (nephrotic syndrome)?

A
  • prednisolone (corticosteroids) and gradually increase dose
  • if resistant to prednisolone –> cyclophosphamide (immunosuppressants)
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18
Q

In which group is membranous glomerulonephritis/nephropathy (nephrotic syndrome) the most common cause of nephrotic syndrome?

A

Most common cause in older adults

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19
Q

Describe the pathophysiology of membranous nephropathy (nephrotic syndrome).

A

Deposition of immune complexes on basement membrane –> damage to podocytes and mesangial cells

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20
Q

What diseases is secondary membranous nephropathy (nephrotic syndrome) commonly associated with? (4)

A
  • malignancy
  • SLE (lupus nephritis)
  • hepatitis B&C
  • autoimmune disease
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21
Q

What would a renal biopsy of membranous nephropathy (nephrotic syndrome) show under light microscopy?

A

Basement membrane thickening (without associated cellular proliferation or infiltration)

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22
Q

What would a renal biopsy of membranous nephropathy (nephrotic syndrome) show under electron microscopy?

A

Spike and dome appearance

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23
Q

Which antibodies is primary membranous nephropathy (nephrotic syndrome) associated with?

A

Anti-phospholipase A2 receptor antibodies (PLA2R)

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24
Q

What other blood result might we see in membranous nephropathy (nephrotic syndrome)?

A

Low T4

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25
Q

How is the response of membranous nephropathy (nephrotic syndrome) to steroids?

A

Low response to steroids

Give: ACEi/ARBs, immunosuppression

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26
Q

In which group is focal segmental glomerulosclerosis (nephrotic syndrome) the most common cause of nephrotic syndrome?

A

Common in Afro-Caribbean population

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27
Q

Describe the pathophysiology of focal segmental glomerulosclerosis (nephrotic syndrome).

A

Sclerosis of glomeruli –> damage and loss of podocytes

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28
Q

What can focal segmental glomerulosclerosis (nephrotic syndrome) be?

A

Primary (idiopathic), secondary or genetic

Differentiating between primary and secondary FSGS is key in determining management

Primary responds to immunosuppression, while secondary treated by reducing intraglomerular pressure (RAAS blockade)

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29
Q

What does light microscopy show in focal segmental glomerulosclerosis (nephrotic syndrome)?

A

Segmental areas of mesangial collapse and sclerosis (affecting some but not all glomeruli)

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30
Q

What does electron microscopy show in focal segmental glomerulosclerosis (nephrotic syndrome)?

A

Effacement of foot processes of podocytes

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31
Q

What is focal segmental glomerulosclerosis (nephrotic syndrome) associated with? (5)

A
  • obesity
  • DM
  • HIV
  • heroin use
  • sickle cell
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32
Q

What does focal segmental glomerulosclerosis (nephrotic syndrome) commonly present with? (3)

A
  • haematuria
  • hypertension
  • reduced renal function
33
Q

What are patients with focal segmental glomerulosclerosis (nephrotic syndrome) often resistant to?

A

Steroids

34
Q

How is focal segmental glomerulosclerosis (nephrotic syndrome) managed?

A

Corticosteroids +/- immunosuppressants

35
Q

What additional signs might you see in patients with diabetic nephropathy (nephrotic syndrome)? (2)

A
  • retinopathy
  • neuropathy
36
Q

What is found in urine in diabetic nephropathy (nephrotic syndrome)?

A

Microalbuminuria (>30mg/day)

37
Q

What can persistent microalbuminuria in diabetic nephropathy (nephrotic syndrome) lead to?

A

If left untreated, will progress to frank proteinuria over 10-15y –> at risk of progressing to end-stage renal disease

38
Q

What will you find on light microscopy in diabetic nephropathy (nephrotic syndrome)? (3)

A
  • mesangial expansion
  • GBM thickening
  • Kimmelstiel-Wilson nodules
39
Q

What does kidney USS show in early stages of diabetic nephropathy (nephrotic syndrome)?

A

Enlarged kidneys (unlike other causes of kidney disease)

40
Q

What are some causes of enlarged kidneys? (4)

A
  • diabetic nephropathy (nephrotic syndrome)
  • autosomal dominant polycystic kidney disease
  • amyloidosis
  • HIV-associated nephropathy
41
Q

How is diabetic nephropathy (nephrotic syndrome) managed? (2)

A
  • diabetic control
  • ACEi/ARB
42
Q

In which group of people is amyloidosis (nephrotic syndrome) seen?

A

Elderly patients

Amyloidosis responsible for 10% of nephrotic syndrome

43
Q

What diseases is amyloidosis (nephrotic syndrome) associated with? (2)

A
  • multiple myeloma
  • chronic inflammatory disease e.g. TB, RA
44
Q

What is the most commonly affected organ in systemic amyloidosis (nephrotic syndrome)?

A

Kidney - deposition of amyloid

45
Q

What are some symptoms of amyloidosis (nephrotic syndrome)? (3)

A
  • breathlessness
  • weakness
  • can cause hepatosplenomegaly
46
Q

What will Congo Red staining show in amyloidosis (nephrotic syndrome)?

A

Apple-green birefringence

47
Q

What can nephrotic syndrome go on to cause? (2)

A
  • hyperlipidaemia - liver compensates for protein loss by increasing albumin synthesis as well as LDL, VLDL and lipoproteins
  • thrombotic disease - loss of antithrombin III, protein C and protein S in urine –> increased hepatic synthesis of procoagulant factors + increased platelet activation
48
Q

How does nephrotic syndrome compare to nephritic syndrome?

A
  • urine contains few cells/casts vs nephritic syndrome –> active urinary sediment (red cells and red cell casts)
  • nephritic syndrome = presence of AKI, hypertension, haematuria
49
Q

What are the clinical features of nephrotic syndrome?

A
  • massive proteinuria (>3.5g/24hr) - may cause foamy urine
  • hypoalbuminaemia (<30g/L)
  • oedema (due to hypoalbuminaemia) - begins as periorbital –> peripheral / pulmonary
  • hyperlipidaemia (low blood protein increases lipid synthesis)
  • hypercoagulable state (loss of ATIII, protein C and protein S and rise in fibrinogen = increased risk of thrombosis)
  • increased risk of infection (loss of immunoglobulins)
50
Q

What are some symptoms of complications of nephrotic syndrome? (3)

A
  • renal vein thrombosis
  • loin pain
  • haematuria
51
Q

What does urine dipstick show in nephrotic syndrome?

A

+++ protein

52
Q

What does 24-hour urine protein show in nephrotic syndrome?

A

> 3.5g in 24h (massive proteinuria)

53
Q

What does urine sediment microscopy show?

A

Fatty casts (dead epithelial cells)

54
Q

Describe serum albumin levels in nephrotic syndrome.

A

Low (leads to oedema)

55
Q

Describe sodium levels in nephrotic syndrome.

A

True hyponatraemia + urinary sodium <20mmol/L - primary renal sodium retention in collecting tubules

56
Q

Describe cholesterol levels in nephrotic syndrome.

A

High

57
Q

What do U&Es show in nephrotic syndrome?

A

Low sodium

58
Q

What is often needed for diagnosis of nephrotic syndrome?

A

Renal biopsy –> light and electron microscopy

59
Q

Compare light and electron microscopy from renal biopsy in minimal change disease vs membranous nephropathy vs focal segmental glomerulosclerosis (nephrotic syndrome).

A
  • minimal change disease: LM normal, EM fusion of podocytes
  • membranous nephropathy: LM BM thickening, EM spike and dome
  • FSGS: LM segmental mesangial collapse and sclerosis, EM effacement of foot podocytes
60
Q

What are some differential diagnoses for nephrotic syndrome? (7)

A
  • nephritic syndrome (AKI, hypertension, red cells and casts in urine, haematuria)
  • minimal change disease (children, normal creatinine and GFR, podocyte effacement/fusion on electron microscopy)
  • membranous nephropathy (PLA2R +ve, thick BM)
  • focal segmental glomerulosclerosis (focal and segmental sclerosis of glomeruli)
  • diabetic nephropathy
  • amyloidosis
  • IgA nephropathy (nephritic disease)
61
Q

What is needed for diagnosis of nephrotic syndrome?

A

Proteinuria (>3.5g/24hr), hypoalbuminaemia (<30g/L) and peripheral oedema

62
Q

How is oedema managed in nephrotic syndrome? (3)

A
  • dietary sodium restriction (50mmol/day)
  • fluid restriction (1L/day)
  • diuretics - spironolactone/furosemide
63
Q

How is proteinuria managed in nephrotic syndrome?

A

RAAS inhibitors:

  • ACE inhibitors (ramipril)
  • ARBs (losartan)
64
Q

What is given as prophylactic anticoagulation in nephrotic syndrome? (2)

A
  • LMWH
  • warfarin
65
Q

How is infection risk managed in nephrotic syndrome?

A

Vaccinations

66
Q

How can we manage minimal change disease?

A

High-dose prednisolone and gradually increase dose

Cyclophosphamide (immunosuppressant) if no response

67
Q

How can we manage membranous nephropathy?

A

ACEi/ARBs, immunosuppression

68
Q

How can we manage focal segmental glomerulosclerosis?

A

Steroids +/- immunosuppression

69
Q

What can we give in early phase of induction therapy (immunosuppression) in nephrotic syndrome?

A

Prophylactic trimethoprim/sulfamethoxazole to prevent pneumocystis pneumonia

70
Q

What are some complications of nephrotic syndrome? (5)

A
  • infection - urinary loss of immunoglobulins
  • VTE - urinary loss of antithrombin III (and protein C and S)
  • hyperlipidaemia - increased hepatic production of lipids (along with albumin) to restore serum oncotic pressure
  • pleural effusion (due to proteinuria –> hypoalbuminaemia –> oedema)
  • CKD and end-stage kidney disease
71
Q

What are the main features of nephritic syndrome (low yield)? (4)

A
  • haematuria
  • proteinuria
  • oedema
  • AKI, hypertension, red cell casts in urine
72
Q

What are some types of nephritic syndrome (low yield)? (2)

A
  • membranoproliferative glomerulonephritis (MPGN)
  • rapidly proliferative glomerulonephritis (RPGN)
73
Q

What causes membranoproliferative glomerulonephritis (low yield)?

A
  • type 1 (90%) - immune complex deposits resulting from chronic infection e.g. hep B/C –> tram track appearance on electron microscopy
  • type 2 - complement deposits e.g. in SLE –> low circulating C3, dense deposits on electron microscopy
74
Q

What is the clinical picture of membranoproliferative glomerulonephritis (low yield)?

A

Mixed picture of nephrotic and nephritic syndrome

75
Q

How do we manage membranoproliferative glomerulonephritis (low yield)?

A

Steroids

76
Q

What is rapidly proliferative glomerulonephritis (low yield)?

A

Proliferation of cells in Bowman’s space –> crescent shape (AKA crescenteric glomerulonephritis)

77
Q

What is type 1 rapidly proliferative glomerulonephritis (low yield)?

A

Goodpasture’s syndrome:

  • mainly nephritic
  • anti-GBM antibodies (autoantibodies against type IV collagen)
  • Sx - pulmonary features (haemoptysis and SOB), nephritic syndrome
78
Q

What is type 2 rapidly proliferative glomerulonephritis (low yield)?

A

Immune-complex mediated:

  • post-streptococcal - nephritic, smoky urine, proteinuria, 1-2wk post throat infection/gastroenteritis –> confirm via anti-Streptolysin O titre, immunofluorescence shows starry sky appearance, low C3 levels
  • IgA nephropathy - 1-2d post GI/resp infection, IgA +ve bloods, young male, recurrent episodes macroscopic haematuria
  • Henoch-Schonlein purpura (IgA vasculitis) - palpable purpuric rash, abdominal pain, polyarthritis, children, IgA +ve bloods
  • SLE - immune complex deposits trigger type III hypersensitivity reaction
79
Q

What diseases come under type 3 rapidly proliferative glomerulonephritis (low yield)?

A

Pauci-immune:

  • cANCA - granulomatosis with polyangiitis (AKA Wegner’s granulomatosis)
    • saddle nose shape, epistaxis, sinusitis
    • consider if ENT, respiratory and kidney issues present in a patient
  • pANCA - microscopic polyangiitis (purpuric rash and pain/numb hands and feet) AND eosinophilic granulomatosis with polyangiitis AKA Churg-Strauss (granulomatous inflammation, asthma-like Sx, eosinophilia)

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