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Gastrointestinal Block > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What is meant by Nephritis?

A

Inflammation of the kidneys

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2
Q

What is Nephritic syndrome?

A

A group of symptoms, NOT a diagnosis, it simply means there is a clinical picture of having inflammation of their kidney

No set criteria

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3
Q

List 4 features of Nephritic syndrome

A
  1. Haematuria (microscopic or macroscopic)
  2. Oliguria
  3. Proteinuria < than 3g/24 hours (any more = nephrotic syndrome)
  4. Fluid retention
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4
Q

What is Nephrotic syndrome?

A

Refers to a group of symptoms without specifying the underlying cause

Has a set criteria

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5
Q

What 4 criteria comprise Nephrotic syndrome

A
  1. Peripheral oedema
  2. Proteinuria > 3g/24 hrs
  3. Serum albumin < 25g / L
  4. Hypercholesterolaemia
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6
Q

What is Glomerulonephritis?

A

An umbrella term for conditions that cause inflammation of or around the glomerulus and nephron

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7
Q

List 4 types of Glomerulonephritis

A
  1. Post streptococcal GN → self limiting disease with good prognosis
  2. Membranoproliferative GN
  3. IgA Nephropathy → most common biopsy diagnosis
  4. Rapidly Progressive GN (2) → most common biopsy diagnosis
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8
Q

What is Interstitial nephritis?

A

Term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney

NOT the same as glomerulonephritis

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9
Q

What is Glomerulosclerosis?

A

The pathological process of scarring of the tissue in the glomerulus

NOT a diagnosis in itself, more a term to describe damage and scarring by other diagnoses

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10
Q

Most treatment of glomerulonephritis are what?

A

usually immunosuppression based

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11
Q

When/how does Post streptococcal GN (PSGN) occur?

A

1 – 3 weeks after a β-haemolytic streptococcus infection,

ie. tonsillitis by Streptococcus pyogenes

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12
Q

Pathogenesis of PSGN

A

Immune complex (IgG, IgM and C3) deposition in the glomeruli

Leads to an acute deterioration in renal function, causing AKI

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13
Q

Light microscopy changes of PSGN

A

Diffuse proliferative glomerulonephritis with prominent endocapillary proliferation with neutrophils

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14
Q

In what clinical scenario would we have a high suspicion of PSGN

A

Evidence of recent tonsillitis caused by streptococcus.

ie. history of tonsillitis, (+) throat swab results, anti-streptolysin antibody titres on blood test

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15
Q

Clinical presentation of PSGN?

A

Can range from asymptomatic microscopic haematuria to nephritic syndrome

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16
Q

Blood findings of PSGN?

A
  • low C3
  • raised ASO titre
17
Q

Management of PSGN

A

Management is supportive, ~80% make a full recovery

  • Antibiotics
  • Antihypertensives and diuretics for complications ie. HTN and oedema
18
Q

What is Membranoproliferative glomerulonephritis (MPGN)?

A

A pattern of glomerular injury on kidney biopsy with characteristic light microscopic changes:

  • hypercellularity
  • thickening of GBM

Histological lesion are a not specific disease, need exploration of cause

19
Q

Pathogenesis of MPGN

A

Thickened GMB:

  • deposition of immune complexes and/or complement factors
  • Interposition of mesangial cells and other cellular elements between GBM and endothelial cell
  • new basement membrane formation

Hypercellularity:

  • Proliferation of mesangial cells and influx of circulating monocytes
  • Leads to lobular appearance of glomerular tuft
20
Q

Classification of MPGN? (2)

A
  1. Types I, II, III - based on EM findings

2.

  • Immune complex mediated (Infections ie. Hep B&C, SLE)
  • Complement mediated
  • Not related to immune complexes or complements
21
Q

Treatment and prognosis of MPGN

A
  1. Treat cause if found – infections, Myeloma etc
  2. Immunosuppression with aggressive disease
  3. Can recur after kidney transplantation
22
Q

IgA Nephropathy is also known as what?

A

Berger’s disease

23
Q

What condition is related to IgA Nephropathy?

A

Henoch-Schonlein Purpura (which is an IgA vasculitis)

24
Q

Pathogenesis of IgA Nephropathy

A

IgA deposits in nephrons of the kidney and causes inflammation (nephritis)

25
Q

What is the pathognomonic finding on renal biopsy of IgA Nephropathy?

A

Histology will show “IgA deposits and glomerular mesangial proliferation”

26
Q

In which age group is IgA nephropathy most prevelant?

A

In teenagers or young adults

27
Q

Clinical presentation(s) of IgA Nephropathy?

A
  1. One or recurrent episodes of gross hematuria, often with an URTI mostly in younger people (40-50%)
  2. Microscopic hematuria and mild proteinuria (30-40%)
  3. Nephrotic syndrome or an acute, rapidly progressive glomerulonephritis (<10%)
28
Q

Clinical Associations with IgA Nephropathy

A
  1. Cirrhosis and other forms of severe liver disease
  2. Coeliac disease
  3. HIV Infection
29
Q

Diagnosis of IgA Nephropathy?

A
  1. Kidney biopsy
  2. Serum IgA levels
  3. Skin biopsy – non specific
30
Q

Treatment of IgA Nephropathy

A

Mild – BP control with ACE-I/ARBs

Moderate - Severe disease – Immunosuppression

31
Q

List the 2 Rapidly Progressive Glomerulonephritises (RPGN)

A
  1. ANCA associated vasculitis
  2. Anti-GBM Disease
32
Q

Clinical Presentation of RPGN

A

Commonly progressive renal impairment, aggressive course needing dialysis

Rarely asymptomatic (SLE, ANCA) with urinary abnormalities (Haematuria and/or proteinuria) or indolent course with maintained renal functions

33
Q

TF is this

A
34
Q

What is ANCA?

A

Antineutrophil Cytoplasmic Antibodies

  • circulating autoantibodies (IgG) against cytoplasm of the neutrophils
  • IIF patterns: cytoplasmic (cANCA) and perinuclear (pANCA)
35
Q

Anti-GBM disease is also know as what?

A

Goodpasture’s

36
Q

Compare Goodpasture’s syndrome vs disease

A

Goodpasture’s syndrome - RPGN with lung haemorrhage

Goodpature’s disease - RPGN with lung haemorrhage and anti-GBM antibodies

37
Q

What are Anti-GBM antibodies?

A

Antibodied directed against an antigen intrinsic to GBM

38
Q

Treatment of RPGN

A
  1. Steroids
  2. Immunosuppression - Cyclophosphamide, Azathioprine, Rituximab
  3. Plasma exchange
  4. Dialysis
38
Q

Blood findings of PSGN?

A

low C3

raised ASO titre

Gastrointestinal Block (26 decks)

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