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Renal > Specific Renal Pathologies > Flashcards

Specific Renal Pathologies Flashcards

1
Q

Difference between primary and secondary glomerular disease

A

Primary - only the kidney is affected

Secondary - other organs are also affected

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2
Q

4 ways that glomerular disease can affect the glomerulus

A

Focal - only some glomeruli
Diffuse - all glomeruli are affected
Segmental - only part of glomerulus
Global - affects all of the glomerulus

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3
Q

5 pathologies of glomerular disease

A

Proliferative - abnormal proliferation of cells - can form a cresent appearance if severe proliferation of macrophages

Mesangial - excess production of mesangial matrix

Membranous disease - basement membrane is damaged and thickened

Membranoproliferative - thickening of glomerular basement membrane and cellular proliferation - usually of mesangial cells

Vasculitis - inflammation of blood vessels

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4
Q

Signs of mild glomerular damage

A

Asymptomatic proteinuria or haematuria

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5
Q

Signs of acute nephritic syndrome

A

Hematuria, acute fall in GFR, sodium and water retention and hypertension

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6
Q

Signs of chronic glomerulonephritis

A

Slow progressive glomerular damage

Proteinuria, haematuria and hypertension

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7
Q

Signs of rapidly progressive glomerulonephritis

A

Rapid renal failure

Oliguria, haematuria and proteinuria

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8
Q

Signs of nephrotic syndrome

A

Heavy proteinuria, hypoalbuminemia and oedema

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9
Q

Effects of glomerulonephritis

A

Inflammation of glomerulus and nephrons

1) Restricts blood flow - compensatory rise in BP
2) Damage to filtration system - protein and blood leak into urine
3) Loss of usual filtration capacity = acute kidney injury

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10
Q

Types of glomerulonephritis x6

A

1) IgA nephropathy
2) Henoch-Schonlein purpura (HSP)
3) SLE
4) Goodpastures
5) Post-streptococcal
6) Rapidly progressive GN

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11
Q

What is IgA nephropathy

- typical presentation

A

Commonest GN in developed world
Macroscopic haematuria 1-2 days after URTI
Young male, intermittent episodic macroscopic haematuria
IgA raised (post-infection)
deposits in mesangial cells

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12
Q

Treatment of IgA nephropathy and HSP

A

BP control with ACE-i

If nephritic presentation - immunosuppression

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13
Q

Prognosis of IgA nephropaty

A

20% develop ESRF in 20years

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14
Q

What is HSP

A

Systemic variant of IgA nephropathy - small vessel vasculitis
Mainly affects children under 10

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15
Q

Features of HSP

A

Purpuric rash on extensor surfaces - ankles, elbows, buttocks
Flitting polyarthritis
Abdominal pain (GI bleeding)
Nephritis

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16
Q

DX of IgA nephropathy and HSP

A

IgA in biopsy and C3 - complement

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17
Q

Prognosis of HSP

A

15% nephritic patients - ESRF

If nephritic and nephrotic - 50% - ESRF

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18
Q

What is Goodpastures disease

A

Autoantibodies to G BM - type 4 collagen

Also affects the lungs - haemoptysis from haemorrhage - especially if they smoke

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19
Q

Presentation of Goodpastures disease

A

Haematuria/nephritic syndrome

AKI may occur within hours of onset

20
Q

Treatment of Goodpastures syndrome

A

Plasma exchange, steroids

Cytotoxics - cyclophosphomide may be needed

21
Q

Prognosis of Goodpastures syndrome

A

If treatment started early then prognosis is good and relapses are unlikely
If renal damage (diffuse therefore likely) then good for renal transplant

22
Q

What happens in post-streptococcal GN

A

Diffuse GN occurs 1-2 weeks after sore throat or skin infection
Antigen deposited on glomerulus - host reaction and immune complex formation
- presents with nephritic syndrome

23
Q

Treatment of post-streptococcal GN

A

Supportive and 95% recover renal function

24
Q

What is rapidly progressive GN?

A

Most aggressive GN - can cause ESRF in days

All have cresents in glomerulus with biopsy

25
Q

Causes of RPGN

A

Immune complex (post-infectious, SLE)
Pauci-immune disease
Anti-GBM disease

26
Q

Triad of nephrotic syndrome

A

Proteinuria, hypoalbuminaemia, oedema

27
Q

Secondary causes of nephrotic syndrome

A

SLE, Hep B/C, Diabetic nephropathy, para-neoplastic, amyloidosis, drug related

28
Q

Drug related nephrotic syndrome

A

NSAIDs, penicillamine, Anti-TNF, gold

29
Q

Investigations in nephrotic syndrome

A

Majority of children its minimal change - therefore no biopsy done
All adults should be biopsied - difficult because hypercoagulable state and oedema

30
Q

Complications of nephrotic syndrome - x3

A

Susceptibility to infection - decreased serum IgG, decreased compliment activity and decreased T cell function - also because of immunosuppressive treatment

Thromboembolism - hypercoagulable state because increased clotting factors and platelet abnormalities - loss of antithrombin III

Hyperlipidaemia - increased cholesterol and triglycerides - thought to be due to increased hepatic lipoprotein synthesis due to low oncotic pressure

31
Q

General treatment of nephrotic syndrome

A

1) Reduce oedema - loop diuretics eg. furosemide 0 fluid and salt restrict
2) ARB or ACEi - reduce proteinuria
3) Anti-coagulate and give statin for cholesterol
4) Vaccinate and treat infections rapidly
5) Treat underlying cause

32
Q

What is minimal change nephropathy?

A

Commonest cause of nephrotic syndrome in children and 20% of adults

Light microscope shows no change - hence name
Electron microscopy shows fusion of podocyte foot processes

33
Q

Presentation of minimal change in children

A

Association with atopy - eczema, asthma and hayfever

Often follows URTI

34
Q

Treatment of minimal change

A

Steroids
If relapses - ciclosporin
1% get ESRF - renal impairment does not occur

35
Q

What is membranous nephropathy

A

Commonest cause of nephrotic syndrome in older patients

Thickening of GBM and subepithelial deposits

36
Q

Causes of membranous nephropathy

A

Usually idiopathic
Secondary to malignancy, Hep B, SLE
Gold or penicillamine

37
Q

Treatment of membranous nephropathy

A

Treat underlying cause
If idiopathic or autoimmune
Steroids and chorambucil or cyclophosphamide

38
Q

Prognosis of membranous nephropathy

A

Minority develop ESRF

39
Q

What is mesangiocapillary glomerulonephritis?

A

Also known as membranoproliferative

Uncommon - occurs mainly in young adults and children

40
Q

Two types of mesangiocapillary glomerulonephritis

A

Immune complex-mediated (underlying cause can usually be found) and complement-mediated

41
Q

Treatment of mesangiocapillary GN

A

Most develop ESRF and there is no treatment
Treat underlying cause if one is found
ACE/ARB for all
Steroids + cyclophosphamide if rapidly progressive

42
Q

What is focal segmental GN?

A

Accounts of 15% of adult nephrotic syndrome

IgM and C3 deposits in affected areas

43
Q

Treatment of focal segmental GN

A

30% respond to steroids

If steroid resistant - try cyclophosphamide or ciclosporin

44
Q

Prognosis of focal segmental GN

A

30-50% go on to develop end stage renal failure

45
Q

Causes of chronic tubulointerstitial nephritis

A

Abnormal anatomy disorders eg. reflux nephropathy and PCKD

In normal anatomy much more rare - 3% and cause is normal analgesic nephropathy

Renal (9 decks)

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