Glomerulonephritis Flashcards

1
Q

What is Glomerulonephritis

A

Inflammation of Glomerulus

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2
Q

Glomerulonephritis is responsible for how much end stage kidney disease

A

15%

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3
Q

Glomerulonephritis classified based on

A

kidney biopsy findings

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4
Q

Glomerulonephritis features

A

Haematuria
Proteinuria
Hypertension
Renal Impairment

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5
Q

Nephritic State

A

Active Urine Sediment: Haematuria, Dysmorphic RBCS, Cellular Casts
Hypertension
Renal Impairment

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6
Q

Nephrotic Syndrome Features (4)

A

Oedema
Nephrotic Range Proteinuria >3.5g/day or 350mg/mmol creatinine
Hypoalbuminaemia: Serum Albumin <35g/L
Dyslipidaemia

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7
Q

What is nephrotic range of proteinuria

A

> 3.5g/day or 350mg/mmol creatinine

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8
Q

Hypoalbuminemia is classified as

A

Serum Albumin <35g/L

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9
Q

Proliferative Glomerulonephritis classified as

A

Excessive numbers of cells in glomeruli. These include infiltrating leucocytes

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10
Q

Non Proliferative Glomerulonephritis classified as

A

Glomeruli look normal or have areas of scarring. They have normal numbers of cells

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11
Q

Which diseases classified as Non Proliferative Nephrotic Glomerulonephritis

A

Minimal Change Disease
Membranous Neuropathy
FSGS

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12
Q

Which diseases classified as Proliferative Nephrotic Glomerulonephritis

A

IgA Nephropathy

Lupus Neuprhtis

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13
Q

Which diseases classified as Proliferative Nephritic Glomerulonephritis

A

Post Infectious GN

ANCA Associated GN

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14
Q

Commonest cause of Glomerulonephritis

A

IgA Nephropathy

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15
Q

IgA Nephropathy characterised by

A

IgA deposition in the mesangium and mesangial proliferation.

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16
Q

IgA Nephropathy most common in

A

2nd and 3rd decade of life with males more commonly affected.

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17
Q

IgA Nephropathy can progress to

A

end stage kidney disease or halving eGFR at 10 years

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18
Q

Presentation of IgA Nephropathy

A

Microscopic haematuria.
Micoscopic haematuria + proteinuria
Nephrotic syndrome
IgA crescentic glomerulonephritis

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19
Q

Post Streptoccal Glomerulonephritis follows

A

10-21 days after throat or skin infection

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20
Q

Post Streptoccal Glomerulonephritis commonly associated with

A

Lancefield Group A Streptocci

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21
Q

Post Streptoccal Glomerulonephritis genetic predisposition

A

HLA-DR, -DP, -DP.

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22
Q

Anti GBM Disease characterised by

A

Circulating Anti GBM

Related to Crescentic Glomerulonephritis

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23
Q

Anti GBM Disease Presentation

A

Nephritis (anti-GBM glomerulonephritis)

Nephritis+ lung haemorrhage (Goodpasture’s syndrome).

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24
Q

Anti GBM Disease Peaks

A

Two peaks: 3rd decade and 6th/7th decade.

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25
Q

Anti GBM Disease Diagnosis

A

demonstrating anti-GBM antibodies in serum and kidney

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26
Q

Anti GBM Disease Treatment

A

aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide.

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27
Q

How does Proliferative Glomerulonephritis present

A

with nephritic state

Haematuria + variable proteinuria + hypertension +/- renal impairment

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28
Q

Proliferative Glomerulonephritis can cause

A

rapid decline needing dialysis

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29
Q

To save nephrons in Proliferative Glomerulonephritis diagnosis

A

Clinical suspicion + immunology screen + renal biopsy

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30
Q

Nephrotic Syndrome Management

A

Treat oedema: salt and fluid restriction and loop diuretics.
Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
Reduce risk of thrombosis: Heparin or Warfarin.
Reduce risk of infection e.g. pneumococcal vaccine.
Treat dyslipidemia e.g. statins.

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31
Q

Minimal Change Disease features

A

Commonest form in children.

Sudden onset of oedema – days.

Remission with steroids (often).

Relapse occurs in two thirds of patients.

32
Q

Minimal Change Disease Treatment

A

Prednisolone – 1mg/kg for up to 16 weeks.

Once remission achieved , slow taper over 6 months.

Initial relapse treated with further steroid course.

Subsequent relapses treated with
Cyclophosphamide
Cyclosporin
Tacrolimus
Mycophenolate mofetil
Rituximab
33
Q

How to treat relapses of minimal change disease

A
Cyclophosphamide
Cyclosporin
Tacrolimus
Mycophenolate mofetil
Rituximab
34
Q

How does Focal and Segmental Glomerulonephritis present

A

Nephrotic Syndrome

35
Q

Pathology of Focal and Segmental Glomerulonephritis

A

tip lesion, collapsing, cellular, perihilar, and not otherwise specified.

36
Q

Focal and Segmental Glomerulonephritis has high chance of

A

end stage kidney disease

37
Q

Focal and Segmental Glomerulonephritis treatment

A

Cyclosporin or Cyclophosphamide or Rituximab

38
Q

Commonest cause of Nephrotic Syndrome in Adults

A

Membranous Nephropathy

39
Q

Serology Markers in Nephrotic Syndrome

A

Anti-phospholipase A2 receptor (PLA2R) antibody

Thrombospondin type 1 domain containing 7A

40
Q

Secondary causes of Nephrotic Syndrome

A

Malignancies
SLE
Rheumatoid arthritis.
Drugs: NSAIDs, gold, penicillamine.

41
Q

Membranous Nephropathy Treatment

A

General measures for at least 6 months.
Immunesuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
Cyclophosphamide and steroids (alternate months) for 6 months.

Tacrolimus.
Rituximab.

42
Q

Prognosis for Membranous Nephropathy good for patients whose

A

proteinuria resolves

43
Q

Membranous Nephropathy can recur in

A

Renal Transplant

44
Q

Non Proliferative Glomeuleonphritis presents with

A

Nephrotic Syndrome

45
Q

Key diagnosis in Non Proliferative Glomeuleonphritis

A

Renal Biopsy

46
Q

What tubule comes off glomerulus

A

proximal

47
Q

Blood enters glomerulus via

A

afferent arteriole

48
Q

All proteins equal to or larger than albumin including immunoglobulins where will they go in glomerulus

A

stay in plasma

will not be filtered

49
Q

Filter barrier in glomerulus contains what 3 things

A

Endothelial cell cytoplasm
basal lamina
podocyte

50
Q

basal lamina is what type of tissue

A

connective

51
Q

filtrate goes into where before proximal tubule

A

bowmen space

52
Q

blood cells and unfiltered proteins exit glomerulus via

A

efferent arteriole

53
Q

Diabetic Glomerulus disease has no what deposition

A

immunoglobulin

54
Q

Glomerulonephtis common presentation

A

Haematuria
Heavy Proteinuria (Nephrotic Syndrome)
Slowly increasing Proteinuria
Acute Renal Failure

55
Q

Haematuria main causes

A

UTI
Urinary Tract Stone
Urinary Tract Tumour
Glomerulonephritis

56
Q

IgA in Iga Nephropathy stains

A

green

57
Q

Which Immunoglobin and Complement component are in all mesangial area of al glomeruli

A

IgA and C3

58
Q

Does IgA get filtered into urine in IgA Nephropathy

A

No it gets stuck in mesangium

59
Q

What gets clogged with antibody in glomerulonephritis

A

Mesangium and not filter membrane

60
Q

what happens to glomerulus basement membrane in membranous glomerulonephritis

A

it gets thickened

61
Q

What immunoglobulin is deposited in membranous glomerulonephritis

A

IgG it gets stuck between basal lamina and podocyte and not filtered into urine

62
Q

In normal glomerulular basement membrane what happens to antibody and albumin

A

stay in plasma and not filtered

63
Q

What happens when IgG activates complement C3

A

it punches holes in filter allowing albumin to be filtered into urine causing nephrotic syndrome

64
Q

which immunoglobulin is too big to be filtered into urine

A

IgG

65
Q

what percentage of those with membranous glomerulonephritis get chronic renal failure within 10 years

A

1/4

66
Q

What are the adhesions to bowmen capsules in diabetic nephropathy

A

glomerulus attempt to stop leak of albumin into urine

67
Q

what is the thickened capillary wall leaking in diabetic nephropathy

A

albumin

68
Q

what compresses capillaries in diabetic neprhopathy

A

increased mesangial matrix

69
Q

what reduces blood flow to glomerulus in diabetic nephropathy

A

arterioles being thick and narrow

70
Q

what are the nodules of mesangial matrix called in diabetic nephropathy

A

Kimmelsteil Wilson Lesion

71
Q

Causes of Crescentic Glomerulonephritis

A

Granulomatosis with Polyangitis (Wegener)
Microscopic Polyarteritis
Antiglomerular Basement Membrane Disease

72
Q

Granulomatosis with Polyangitis affects

A

Vasculitis which affects kidneys, nose and lungs

73
Q

Serum tests in wegerers shows

A

presence of anti neutrophil cytoplasmic antibodies (ANCA)

74
Q

ANCA are not deposited where

A

in kidney

75
Q

ANCA are directed against what in glomerular disease

A

proteinase 3 and myeloperoxidase

76
Q

If Wegener’s (Granulomatosis with Polyangitis) is left untreated what happens

A

Fatal

77
Q

By giving Cyclophosphamide for Wegener Granulomatosis with Polyangitis) what happens?

A

75% complete remission