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`Nephrology > Nepthritic syndrome > Flashcards

Nepthritic syndrome Flashcards

1
Q

Nephritis syndrome : Causes

A
  1. Children and Adolescents
    - IgA nephropathy
    - Post streptococcal glomerulonephrotos
    - Haemolytic uraemia syndrome
  2. Adults
    - Systemic lupus erythematosis
    - Goodpasture’s syndrome
    - Rapidly progressive glomerulonephritis
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1
Q

Nephritic syndrome : definition

A
  1. Diseased caused by inflammation and damage to glomeruli of kidney
  2. Glomeruli become more permeable -> Allow RBCs into the urine -> Haematuria

3 . Clincial features :
* Haemturia
* Oliguria
* Oedema
* Hypertension

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2
Q

Nephritis syndrome : Clinical signs and symptom

A
  1. Haematuria / Proteinuria : Damaged, Permeable glomeruli
  2. Odaema, Hypertension : Decreased glomerular filtration rate
  3. Uraemia : less waste product excreted
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3
Q

Post streptococcal glomerularnephritis : definition

A
  1. Inflammation of glomeruli, complication of bacterial infection
  2. Arises several weeks after : Group A beta haemolytic streptococcus infection
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4
Q

Post streptococcal glomerularnephritis : Pathophysiology

A
  1. Type III hypersensitivity reaction
  2. IgG/IgM antibodies bind to bacterial antigens } form immune complex in the blood stream.
  3. Complex deposits in the glomerular basement membrane
  4. Immune complex deposits trigger immune reaction -> inflammatory cells /Complement system recruited -> Basement membrane damage
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5
Q

Post streptococcal glomerularnephritis : Cause

A

Group A beta haemolytic streptococcus infection

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6
Q

Post streptococcal glomerularnephritis : Risk factors

A

Children - 6 weeks following Impetigo, 1-2 weeks after a throat infection

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7
Q

Post streptococcal glomerularnephritis : Complication

A
  1. Post-streptococcal glomerulonephritis causes progress to acute, diffuse proliferative glomerulonephritis
  2. Renal failure
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8
Q

Post streptococcal glomerularnephritis : Investigation

A

1 .Bloods
Antibodies against group A strep : Anti streptolysin O antibodies

2 . Renal biopsy
* Light microscopy - mesangial proliferation
* Electron microscopy : Subepithelial deposits of immune complexes ‘Humps’
* Immunofluorescence : ‘Starry sky’ granular deposits of IgG complement in the basement membrane of the mesangium

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9
Q

Good pasture’s syndrome : Definition

A

Goodpasture syndrome is an autoimmune disease in which the immune system attacks the A3 chain of Type IV collagen present in the basement membrane

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10
Q

Good pasture’s syndrome : Pathophysiology

A
  1. Auto-antibody igG bind to A3 chain of type IV collagen and activate the complement system
  2. Inflammation and damage to the basement membrane of the kidney and the lungs.
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11
Q

Good pasture’s syndrome : Risk factor

A
  1. Environmental
    Damage to collagen molecules - exposing antigenic regions of A3 chain - Infection, smoking, occupational risk
  2. Genetic - HLA-DR15 strong genetic susceptibility
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12
Q

Good pasture’s syndrome : Incidence

A

20-30 years

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13
Q

Good pasture’s syndrome : Clinical features

A

Pulmonary manifestations occur before renal ones
1. Damaged alveolar basement membrane : Cough, haemoptysis and dyspnea
2. Damaged GBM of the kidneys : Nephritic syndrome

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14
Q

Good pasture’s syndrome : Investigations

A

Renal biopsy
1. Light microscopy : Crescentric glomerularnephritis
2. Electron microscopy : Diffuse thickening of the glomerular basement membrane
3. Immunofluorescence : Linear deposition along basement membrane

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15
Q

Good pasture’s syndrome : Management

A
  1. Immunosuppressant : Corticosteroid, Cyclophosphamide
  2. Plasmapheresis
16
Q

Rapidly progressive glomerulonephritis : definition

A

Inflammation of the nephrons - crescent shaped proliferation of cells in the Bowman’s capsule
* This leads to renal failure within weeks - months

17
Q

Rapidly progressive glomerulonephritis : Pathophysiology

A
  1. Inflammation damages the GBM
  2. Inflammatory mediators enter the Bowman’s space
  3. Trigger expansion of thin epithelial layer of cells into thick, crescent moon shape
18
Q

Rapidly progressive glomerulonephritis : Causes

A

1 .Primary : Idiopathic

2 .Secondary
* Type 1 : anti GBM antibodies
-Goodpasture syndrome

  • Type II : Immune complexes deposition
    -Poststreptococcal glomerulonephritis
    -Lupus
    -IgA nephropathy
  • Type III : ANCA antibodies in the blood
    -Vasculitis : Wegener’s granulomatosis etc
19
Q

Rapidly progressive glomerulonephritis : Complication

A

If untreated - Rapid progression to acute renal failure

20
Q

Rapidly progressive glomerulonephritis : Diagnosis

A
  1. Light microscopy : crescent shaped glomeruli dueto proliferation of epithelial cells in bowmans capsule
  2. Immunofluorescence - differentiate types of RPG
    * Type 1 : Linear pattern
    Anti GBM Antibodies bind to collagen of the glomerular basement membrane
    * Type II : Granular pattern
    Result of immune complex deposition int he sub endothelium
    * Type III : negative
    No antibodies or immune complex deposition } only associated with ANCA in the blood
21
Q

Rapidly progressive glomerulonephritis : Incidence

A

Affects adults in their 50s and their 60s
Typically has a poor prognosis if not treated early.

22
Q

Which is the most common nephropathy worldwide?

A

IgA nephropathy / Berger disease

23
Q

IgA nephropathy : Definition

A

Abnormal IgA forms and deposits in the kidneys resulting in kidney damage

24
Q

Where are igA antibodies found in the body?

A

IgA is the main antibody found in breast, tears, saliva and respiratory and gentiourinary tract

25
Q

IgA nephropathy : Pathophysiology

A
  1. Abnormal IgA form
    * Abnormal IgA forms due to glycosylation
    * Glycosylated IgA antibodies cannot be identified by the immune system - leading them to accumulate and not degraded.
  2. Immune system responds
    * Immune system generates IgG antibodies which targets the abnormal IgA
    * IgG antibodies bind to abnormal IgA and forms immune complexes, this travels through the blood stream and deposits in the kidneys.
  3. Kidney injury and inflammation
    * Type 3 Hypersensitivity
    * Immune complexes deposits in the mesangium
    * Activates the complement pathway and inflammatory response resulting in glomerular injury.
26
Q

IgA nephropathy : Clinical features

A
  1. Presents in childhood, normally young males with recurrent haematuria (v. Rarely proteinuria)
    * develops during an infection involving mucosal lining of the GI or respiratory tract, these infections ramp up IgG anti-glycan formation.
  2. Nephritic syndrome - Proteinuria, haematuria, Hypertension
27
Q

IgA nephropathy : Investigations

A
  1. Light microscopy
    Mesangial proliferation and immune complexes in the mesangium
  2. Electron microscopy
    -Immune complexes deposited in the mesangium
  3. Immunofluorescence
    -Mesangial IgA deposits
28
Q

IgA nephropathy : Management

A
  1. Isolate haematuria or minimal proteinuria and normal eGFR : no tx needed
  2. Persistent proteinuria + reduced eGFR : Ace inhibitors, also helps to manage hypertension and proteinuria
  3. Active disease : Immunosupression with corticosteroids

`Nephrology (12 decks)

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