Glomerulonephritis Flashcards

1
Q

Define glomerulonephritis.

A

Glomerulonephritis encompasses a number of conditions which

  • are caused by pathology in glomerulus
  • present with haematuria, proteinuria or both
  • are diagnosed on renal biopsy
  • cause CKD
  • can progress to kidney failure (except with minimal change disease - MCD)
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2
Q

What are the 2 main consequences of glomerular inflammation and how do these present?

A
  1. Loss of barrier function –> proteinuria (mild to nephrotic syndrome) and haematuria (mild to macrocytic)
  2. Loss of filtering capacity –> reduced excretion causing accumulation of waste products (AKI)
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3
Q

What are the risk factors for glomerulonephritis?

A
  • Group A beta-haemolytic strep
  • Resp infection
  • GI infection
  • Hep B and C
  • Infective endocarditis
  • HIV
  • SLE
  • Systemic vasculitis
  • Hodgkin’s lymphoma
  • Lung cancer
  • Colorectal cancer
  • non-Hodgkin’s lymphoma
  • Leukaemia
  • Thymoma
  • Haemolytic uraemic syndrome
  • Drugs - penicillamine, gold sodium thiomalate, non-steroidal anti-inflammatory drugs, captopril, mitomycin C, cocaine, and anabolic steroids.
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4
Q

Briefly describe the range of glomerular diseases.

A

Spectrum ranges from proteinuria (nephrosis) to haematuria (nephritis).

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5
Q

List 5 causes of glomerulonephritis.

A
  1. IgA nephropathy - commonest cause worldwide
  2. HSP - variant of IgA with systemic involvement (skin, connective, GI, scrotum)
  3. Anti-GBM (Goodpasture’s) - crescentic GN, auto-Ab to type IV collagen. Bind to alveolar BM –> lung haemorrhage.
  4. Post streptococcal GN - 1-12 weeks after throat/skin infection
  5. Pauci-immune - commonest cause of GN - +ve ANCA but negative immunofluorescence
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6
Q

What are the signs and symptoms of glomerulonephritis?

A
  • Asymptomatic haematuria +/- proteinuria
  • Nephrotic syndrome: heavy proteinuria, hypoalbuminuria, fluid retention
  • Nephritic syndrome : haematuria, proteinuria, fall in GFR, salt and water retention and hypertension
  • Rapidly progressive GN - rapid loss of renal function such as ESKD within weeks or months
  • Chronic GN - slow deterioration in renal function, over several years with haematuria, proteinuria, hypertension.
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7
Q

What investigations would you do for glomerulonephritis?

A

Oliguria, urine casts, crescents (if AKI results),

  • Bloods
    • FBC - normocytic normochromic anaemia
    • Lipid profile - hyperlipidaemia or normal
    • U&Es, CRP, Complement (C3, C4)
    • Autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM), blood culture, ASOT
    • Serum albumin - low
    • LFTs - elevated e.g. in Hep C or B
    • GFR - reduced in CKD
  • Urine MC&S - Bence Jones protein, RBC casts (+dysmorphic RBCs) , haematuria, proteinuria, leukocytes
  • A:CR (spot urine albumin: creatinine ratio) - normal urine ACR is <220mg/mmol. May be raised in GN.

Imaging

  • CXR - pulmonary haemorrhage
  • Renal USS - size and anatomy for biopsy, may be small in chronic process
  • Biopsy - renal biopsy required for diagnosis
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8
Q

What are the 4 types of severity of glomerulonephritides?

A
  • Minimal change
  • Diffuse - affecting all glomeruli
  • Focal - affecting only some glomeruli
  • Segmental - only affecting parts of an affected glomerulus
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9
Q

What is the management of GN?

A

Management: not on Sofia

  • Refer specialist
  • BP management – <130/80
  • ACE-I or ARB – reduce proteinuria and preserve renal function
  • Steroids/immunosuppression
  • Treat underlying cause
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10
Q

Why are ACEi/ARB useful in GN?

A

Reduce intraglomerular pressure by inhibiting AGII efferent vasoconstriction

Usually angiotensin acts to constrict both afferent and efferent arterioles but preferentially efferent.

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11
Q
A
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12
Q

What are the types of crescentic glomerulonephritis?

A

Immune complex associated

Anti GBM

Pauci-immune

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13
Q

What are the types of immune complex associated glomerulonephritis?

A

SLE

IgA nephropathy

Post-infectious glomerulonephritis

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14
Q

What are the types of non-immune complex associated glomerulonephritis? (nephrotic syndrome)

A

MCD

FSGS

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15
Q

What are the differences between treatment of MCD and FSGS?

A

MCD - generally responds to immunosuppression

FSGS - less likely to respond to immunosuppression

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16
Q

What is the antibody target in MGN?

A

Phospholipase A2

17
Q

How common is diabetic nephropathy?

A

Affects 30-40% of diabetics

18
Q

What are the stages of diabetic nephropathy?

A

Stage 1 - thickened BM

Stage 2 - more mesangial matrix

Stage 3 - nodular lesions (Kimmelstiel Wilson)

Stage 4 - advanced glomerulosclerosis

19
Q

What is the most common glomerulonephritis?

A

IgA nephropathy - from immune complex deposition

20
Q

What is the management of IgA nephropathy?

A
  • Observation and follow up = isolated haematuria, no or minimal proteinuria (<500mg/day), and a normal GFR
  • ACEi = if persistent proteinuria (>500mg/day), a normal or only slightly reduced GFR
  • Corticosteroids = if there is active disease (e.g. falling GFR) or failure to respond to ACEi
21
Q

What is the prognosis with IgA nephropathy?

A

25% → ESRF

Frank haematuria is a good prognostic factor

Poor prognosis if male, >2g/day proteinuria, HTN, smoking, hyperlipidaemia, ACE genotype DD

22
Q

What is the management of MCD?

A

Oral corticosteroids - helps in 80% of cases

Cyclophosphamide if steroid resistant

23
Q

What is the prognosis with MCD?

A
  • 1/3 have just one episode
  • 1/3 have infrequent relapses
  • 1/3 have frequent relapses which stop before adulthood
24
Q

What is the management of FSGS?

A
  • Steroids +/- immunosuppressants
25
Q

What is the prognosis with FSGS?

A

Untreated FSGS has a < 10% chance of spontaneous remission

26
Q

What is the management of membranous glomerulonephritis?

A

ACEi or ARB - reduce proteinuria and improve prognosis

Immunosuppression (corticosteroid AND another agent)- only for those with severe disease; many improve without this. Corticosteroid alone not effective.

Anticoagulation - for high risk patients

27
Q

What is the prognosis with MGN?

A
  • one-third: spontaneous remission
  • one-third: remain proteinuric
  • one-third: develop ESRF
28
Q

What is the management of diabetic nephropathy?

A

Dietary protein restriction

Tight glycaemic control

BP control <130/80

ACEi or ARB - start when ACR is 3mg/mmol

Statin - controls dyslipidaemia

29
Q

What is the management of post-streptococcal glomerulonephritis?

A

Penicillin G - eradicates the nephrogenic strain

Manage hypertension and oedema

30
Q

What is the prognosis with post-streptococcal glomerulonephritis?

A

>90% of children make a full recovery

Adults have a worse outcome due to renal function impairment

31
Q

What is the management of anti-GBM?

A

Plasmapheresis

Steroids

Cyclophosphamide

32
Q

What are the complications of anti-GBM?

A

One of the main complications is pulmonary haemorrhage.