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Year 2 - Renal > Pathology + clinical of glomerular disease > Flashcards

Pathology + clinical of glomerular disease Flashcards

1
Q

Define glomerulonephritis

A

Umbrella term for diseases of the glomerulus (can be inflammatory OR non-inflammatory)

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2
Q

Function of podocytes

A

Line and wrap the outside of the glomerular capillaries with their foot like processes
-help prevent proteins/other large molecules from being filtered out of blood into bowman’s space

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3
Q

Function of mesangial cells

A

Lie between the loops of glomerular capillaries and hold them together, supporting them

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4
Q

What things don’t get filtered into bowman’s space from the afferent arteriole

A

Blood cells

Albumin/ immunoglobulins (antibodies)/ other large proteins

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5
Q

Common aetiology of glomerulonephritis

A

Leukocyte infiltration, antibody deposition, and complement activation

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6
Q

Glomerulonephritis commonly presents in the following 4 ways (separate presentations)

A

Haematuria - usually microscopic

Heavy proteinuria - leg oedema

Slowly increasing proteinuria

Acute renal failure

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7
Q

Main causes of haematuria (4 - 3 common, 1 less common)

A

Urinary tract

  • infection
  • stone
  • tumour

Glomerulonephritis (LESS COMMON CAUSE)

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8
Q

Pathophysiology of IgA nephropathy (a type of glomerulonephritis)

A

Idiopathic but associated with formation of circulating IgA immune complexes that are prone to depositing in the mesangium of the glomerulus –> irritates the mesangial cells and causes them to proliferate which produces a bigger mesangial matrix –> disrupts filtering ability –> blood and proteins leak into urine

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9
Q

IgA nephropathy (a type of glomerulonephirits) appears within 48 hours of what

A

URTI or gastroenteritis

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10
Q

IgA nephropathy presents as nephritic syndrome which means they present with what urine findings (2)

A

VISIBLE haematuria

Proteinuria - less significant than the haematuria

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11
Q

Prognosis of IgA nephropathy

A

Only self limiting, usually return to normal

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12
Q

Investigations of IgA nephropathy + findings (3)

A

Urinalysis - urine dipstick +ve for blood

Urine microscopy - shows RBCs, RBC casts

RENAL BIOPSY (DEFINITIVE)

  • light microscopy - shows enlarged mesangial matrix
  • immunofluoroscence - lights up IgA deposits
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13
Q

3 types of haematuria

A

Invisible

  • microscopic
  • dipstick

Visible (macroscopic)

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14
Q

Presentation of membranous nephropathy (think: it’s a non-proliferative form of GN)

A

Nephrotic syndrome

  • oedema
  • proteinuria –> FOAMY urine
  • hypoalbuminaemia
  • hyperlipidaemia –> xanthelasma
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15
Q

Pathophysiology of PRIMARY membranous nephropathy/glomerulonephritis (commonest cause of nephrotic syndrome in ADULTS)
-what happens to GBM

A

Idiopathic/autoimmune mechanism
-IgG immune complex deposits in the glomeruli –> activates complement system which recruits inflammatory cells to the area which promote inflammation and THICKENING OF GBM –> podocytes become effaced (erased) allowing things to leak into urine

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16
Q

Membranous nephropathy where the glomerular basement membrane becomes very leaky because podocytes are lost, large weight molecules like albumin are easily lost so it’s one of the biggest causes of what syndrome

A

Nephrotic syndrome

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17
Q

2/3 cases of membranous nephropathy are primary (idiopathic), 1/3 are secondary to (4)

A

Autoantibodies in response to underlying conditions
Autoimmune diseases- SLE
Hepatitis
Lung/colon cancer

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18
Q

Primary membranous nephropathy is IDIOPATHIC

but has been found to be associated with circulating auto-antibodies to what receptor to form immune complexes

A

Phospholipase A2 receptor (PLA2R) on podocytes

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19
Q

What test must you do first before renal biopsy

A

Clotting screen - to determine risk of bleeding from the biopsy

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20
Q

Pathophysiology of diabetic nephropathy* (3)

*Defined by characteristic mesangial expansion, GBM thickening, and glomerular sclerosis leading to the development of Kimmelstiel-Wilson nodules

A

Due to excess blood glucose OVER-RIDING renal threshold for glucose –> glycosuria

High BG from untreated DM causes high BP which puts strain on the tiny glomerular capillaries as it causes mesangium to expand through stretch

High BG also causes glycation of proteins which stimulate expansion and THICKENING OF GBM –> hyaline arteriosclerosis –> becomes LEAKY

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21
Q

Glomerular filtration barrier consist of 3 layers

A

fenestrated endothelium, the glomerular basement membrane, and the epithelial podocytes

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22
Q

In diabetic nephropathy, what happens to the mesangium

A

expands and proliferates which compresses the glomerular capillaries

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23
Q

In diabetic nephropathy, mesangial matrix expansion starts to invade the glomerular capillaries and produces nodules of excess mesangial matrix called

A

Kimmelstiel-Wilson nodules,

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24
Q

What is crescentic glomerulonephritis (aka rapidly progressive GN)

A

Just a name used to describe forms of glomerulonephritis that are characterised by CRESCENT SHAPED PROLIFERATION OF CELLS in bowman’s space

usually are RAPIDLY PROGRESSIVE forms of GN and associated with a poor prognosis

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25
Q

Crescentic glomerulonephritis (a name used to describe forms of glomerulonephritis that are characterised by CRESCENT SHAPED PROLIFERATION OF CELLS in bowman’s space)

What composes the crescents

A

Cellular proliferation and macrophages

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26
Q

What is granulomatosis with polyangiitis (aka Wegener’s granulomatosis)

A

A form of crescentic glomerulonephritis

-is a systemic vasculitis that involves inflamed vessels in the kidneys, lungs

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27
Q

Autoantibody tested for in granulomatosis with polyangiitis (aka Wegener’s granulomatosis)

A

anti-neutrophil cytoplasmic antibodies (ANCA)

28
Q

Sources of haematuria

A 
Kidney
Ureter
Bladder
Prostate
Urethra
29
Q

Haematuria seen in nephritic or nephrotic syndrome more

A

nephritic

30
Q

Nephrotic syndrome involves the loss of a lot of …, whereas nephritic syndrome involves the loss of a lot of …

A

protein

blood

31
Q

Nephrotic syndrome (just describes a collection of symptoms) is characterised by (4)

A

Proteinuria - LOTS

Hypoalbuminaemia - albumin lost in urine

Severe oedema (–> weight gain) - albumin lost in urine so decreased oncotic pressure so moves out blood vessels

Hyperlipidaemia

32
Q

Nephritic syndrome (just describes a collection of symptoms) characterised by (4)

presence of acute kidney injury (renal dysfunction), hypertension, and an active urinary sediment (red cells and red cell casts).

A

Haematuria - LOTS

Proteinuria - MUCH LESS THAN NEPHROTIC SYNDROME

Hypertension

Low urine volume - renal impairment

33
Q

Hypertension is associated more with nephritic or nephrotic syndrome

A

nephritic (lots of haematuria)

34
Q

Proliferative glomerulonephritis vs non-proliferative glomerulonephritis

A

Proliferative - excessive numbers of cells in the glomeruli, e.g. infiltrating leukocytes

Non-proliferative - glomeruli look normal/may have scarring but normal numbers of cells

35
Q

Nephrotic syndrome primary* (3) and secondary causes (2)

These are NON-PROLIFERATIVE forms of GN

A

Primary

  • Minimal change disease
  • Focal segmental glomerulosclerosis (FSGS)
  • Membranous nephropathy

Secondary

  • DM (diabetic nephropathy)
  • SLE
36
Q

Nephritic syndrome causes* (4)

*These are PROLIFERATIVE forms of GN

A

Post-streptococcal glomerulonephritis - is a diffuse proliferative GN

IgA nephropathy - is a focal proliferative GN

Crescentic glomerulonephritis (or rapidly progressive)

Membranoproliferative glomerulonephritis

37
Q

Post-streptococcal GN (a form of proliferative GN) is preceded by an infection with what

A

usually group A streptococci - strep pyogenes

38
Q

Investigations of glomerulonephritis in general (4)

A

Urinalysis - urine dipstick, urine microscopy

U+Es

FBC

Renal biopsy

  • light microscopy with H&E stain
  • electron microscopy
  • immunofluorescence
39
Q

Diagnosis of post-streptococcal GN

A

Symptoms/signs of GN -proteinuria, haematuria, fever

History of recent throat strep infection

40
Q

Treatment of post-streptococcal GN

A

Gets better on its own so just SUPPORTIVE measures

  • limit salt and fluid intake - MAIN (may just need this)
  • diuretic - to reduce oedema
  • BP control - ACE/ARB

+/- antibiotics
- to treat any remaining streptococcus

41
Q

Crescentic glomerulonephritis (aka rapidly progressive GN) is the most severe form of proliferative GN

Name 2 examples of crescentic glomerulonephritis

A

Granulomatosis with polyangiitis (Wegner’s granulomatosis) - vasculitic

Anti-glomerular basement membrane disease (goodpasture’s syndrome)

42
Q

Goodpasture’s syndrome (anti-glomerular basement membrane disease) is associated with what autoantibody

A

Anti-glomerular basement membrane antibody
-attacking proteins in the GBM

Affects LUNGS before kidneys

43
Q

Symptoms/signs of granulomatosis with polyangiitis (a type of crescentic glomerunephritis)

  • constitutional
  • resp
  • cutaneous
A

Constitutional symptoms - fever, malaise, anorexia, weight loss

Resp symptoms/signs - e.g. SOB, crackles

Cutaneous - rash/lesions

44
Q

Treatment of granulomatosis with polyangiitis (a type of crescentic glomerunephritis) (2)

A

Immunosuppression

  • high dose steroids
  • Cyclophosphamide - chemo drug; cytotoxic
45
Q

Treatment of Goodpasture’s syndrome (anti-glomerular basement membrane disease) (3)

A

Immunosuppression

  • high dose steroid
  • Cyclophosphamide
  • Plasmapheresis (plasma exchange)
46
Q

Principle of crescentic glomerulonephritis (e.g. granulomatosis with polyangiitis, anti-GBM disease) treatment is IMMUNOSUPPRESSION

What immunosuppressants may be given (3)

A

IV high dose steroids
Cyclophosphamide - chemo drug
Plasma exchange

47
Q

Principles of management of nephrotic syndrome due to glomerulonephritis (2 principles; 1st principle has 3 things)

A

General measures

  • treat oedema - with loop diuretic
  • treat hypertension - with ACEI/ARB
  • treat high cholesterol - with statin

Specific therapy towards the underlying non-proliferative GN
-usually STEROID

48
Q

Minimal change disease is the commonest type of non-proliferative GN in

(this type accounts for 90% nephrotic syndrome cases in these people)

A

children

49
Q

Minimal change disease (a form of non-proliferative GN) symptoms/signs

A

Nephrotic syndrome

  • oedema - SUDDEN ONSET
  • proteinuria
  • hypoalbuminaemia
  • hyperlipidaemia
50
Q

Pathological finding of minimal change disease

A

Loss of podocyte foot processes

51
Q

Treatment of minimal change disease (2)

  • medical - RESPONDS VERY WELL TO THIS
  • lifestyle
A

Oral prednisolone - repsonds very well to this

Reduce oedema - with low salt diet and fluid restriction

52
Q

What is focal segmental glomerulosclerosis + initiating factor

A

A chronic form of non-proliferative GN that affects PARTS (SEGMENTAL) of SOME (FOCAL) glomeruli –> damage, scarring

Initiating factor - chronic damage to foot processes of podocytes –> EFFACEMENT

53
Q

Primary/secondary causes of focal segmental glomerulosclerosis

A

Primary - idiopathic

Secondary - HIV, reflux nephropathy

54
Q

If there’s lots of protein in urine like in severe nephrotic syndrome, what is the appearance of the urine

A

foamy

55
Q

Which types of glomerulonephritis have high chance of progression to end stage kidney disease

A

Proliferative
-crescentic glomerulonephritis

Non-proliferative
-focal and segmental glomerusclerosis

56
Q

Histological findings in focal segmental glomerulosclerosis

A

segmental areas of mesangial collapse and sclerosis

57
Q

Symptoms/signs of focal segmental glomerulosclerosis

A

Non-proliferative form so presents as nephrotic syndrome (the 4 characteristics)

Foamy urine

58
Q

Treatment of focal segmental glomerusclerosis (5)

A

Supportive measures

  • salt + fluid restriction diet
  • loop diuretic
  • ACEI/ARB
  • statin

Prednisolone - but often resistant to steroids

59
Q

Steroid treatment is often resistant in focal segmental glomerusclerosis so what alternative immunosuppressants may be given

A

Ciclosporin

Cyclophosphamide

60
Q

Definitive investigation of focal segmental glomerulosclerosis

A

Renal biopsy

61
Q

Commonest cause of nephrotic syndrome in adults v children

A

Adults - membranous nephropathy

Children - minimal change disease

62
Q

Treatment of membranous nephropathy in
-low risk (3)
-moderate-high (above + 2)
of end stage renal failure

A

Supportive measures for at least 6 months

  • reduce oedema - loop diuretic
  • BP control - ACEI/ARB
  • cholesterol control - statin

If moderate/high risk then PLUS
-steroid + cyclophosphamide

63
Q

In membranous nephropathy

  • light microscopy shows what
  • immunofluorescence shows what
A

THICKENED GBM

  • electron dense deposits in the subepithelial space
  • IgG deposits throughout capillary walls
64
Q

Management principles of any form of glomerulonephritis

  • supportive (4)
  • specific
A

Supportive measures

  • restrict salt and fluid intake
  • reduce oedema - loop diuretic
  • BP control - ACEI/ARB
  • cholesterol control - statin

+/- Immunosuppression - usually prednisolone

65
Q

Post streptococcal GN occurs how long after the URTI compared to IgA nephropathy

A

post streptococcal - about 2 weeks after URTI

IgA - about 2 days after

Year 2 - Renal (21 decks)

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