Renal pathology Flashcards

1
Q

What are the purposes of renal biopsy? (3)

A

Renal biopsy - aim depends on the presentation, usually:

  • to establish the diagnosis
  • to assess the severity of the renal disease
  • to assess the amount of irreversible damage
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2
Q

What type of kidney sections do we use in kidney biopsy?

A

Thin sections (3um) -> thick will give false positive impression of increased cellularity

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3
Q

What routine stain is used to identify different cells in the kidney?

A

H&E stain

(Haemotoxylin and Eosin)

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4
Q

What are PAS and silver stains used for?

A

To highlight basement membrane and connective tissue

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5
Q

What stain is used for amyloid?

A

Congo red stain

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6
Q

What is elastin stain used for?

A

to examine the vessels

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7
Q

What are immunofluorescence or immunohistochemistry techniques used for?

A

Used to identify immune complexes types and localisation

e.g. anti-GBM, IgA, IgG, complement

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8
Q

What is electron microscopy technique used for?

A
  • immune complex - nature and localisation
  • glomerular membrane abnormalities
  • foot process effacement /pl zamazanie/
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9
Q

In general, what classification of renal pathology is there?

A
  • Primary renal disease -> disease originating from the kidney (e.g. glomerulonephritis)
  • Secondary renal disease -> disease originating from elsewhere but manifesting itself in the kidney (e.g. DM)
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10
Q

Clinical presentation of Nephrotic vs nephritic syndrome

A
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11
Q

IgA nephropathy

  • what happens
  • what’s the diagnosis
A

IgA nephropathy

  • the most common type of glomerulonephritis
  • Abnormal IgA is formed and deposited in the capillaries of glomeruli
  • Diagnosis: renal biopsy (to confirm Dx and decide on type of Rx)
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12
Q

What can we see on histology report of IgA nephropathy?

A
  • mesangial expansion
  • endocapillary proliferation
  • other features: e.g. crescents and thrombosis

*proliferation - a lot more nuclei in the segment; swelling of the cells

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13
Q

What are other findings (outside of glomerulus) in IgA nephropathy?

A
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14
Q

What is the difference in chronic vs acute damage to the kidney)?

A
  • Acute -> if we Rx we may reverse the changes (aggressive treatment); Rx active disease to stop the inflammatory process
  • Chronic -> if fibrosis has occurred, we would not be able to Rx it (no point to Rx aggressively as pt will get side effects but it would not change anything)
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15
Q

What is the most common cause of proteinuria and nephrotic syndrome in adults?

A

Membranous glomerulonephritis

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16
Q

What are the two types of membranous glomerulonephritis?

A
  • Primary membranous glomerulonephritis -> idiopathic (we do not know what causes abnormal immunoglobulin deposition in glomeruli)
  • Secondary membranous glomerulonephritis -> something else causes abnormal immunoglobulin deposition in glomeruli
17
Q

Causes of membranous glomerulonephritis

A
  • Infections: Hep B, Hep C, Syphilis etc.
  • Drugs: NSAIDs
  • Neoplasms: GI, renal ca, lung, stomach, breast etc.
18
Q

Why do we need to differentiate between primary/secondary membranous glomerulonephritis in terms of Rx?

A

This is because if the cause is an infection or neoplasm - by starting immunosuppression, we would make a disease worse

*in secondary membranous glomerulonephritis -> we need to aim to treat an underlying cause

19
Q

What’s histological characteristic of membranous glomerulonephritis?

A

Thickening of glomerular membrane

*thickening = due to IgG deposition along glomerular membrane

20
Q

What is seen on the silver stain in membranous glomerulonephritis?

A

Fenestration or spikes

*these are ‘holes’ in the glomerular membrane -> as silver stain stains only membrane and collagen, it would not stain IgG deposits on the membrane

21
Q

Is there any investigation to differentiate between idiopathic/ primary and secondary membranous glomerulonephritis?

A
22
Q

Examples of secondary renal diseases (3)

A
  • diabetic nephropathy
  • renal amyloidosis
  • systemic hypertension -> causing renal damage
23
Q

Diabetic nephropathy

  • onset of a disease
  • most common symptoms
  • what to do to delay the progression
A

Onset: 10 year or more of history of DM

Most common symptoms: proteinuria

To delay the progression: control hyperglycaemia and hypertension

24
Q

What histological changes are seen in diabetic nephropathy (in glomerulus)?

A

Glomeruli:

  • nodular sclerosis
  • diffuse thickening of glomerular membrane -> mesangium will expand (becomes fibrotic) and forms nodules -> so filtration process is affected

*no splitting or spike formation -> as no immunoglobulin deposition

25
Q

What are other findings (apart from these in glomerulus) in diabetic nephropathy?

A

These changes happen due to the increased amount of proteins in the urine -> irritation of the tubules and damage to the epithelium

  • Interstitial fibrosis, chronic inflammatory cell infiltrate, tubular atrophy
  • vessels affected: thickening and sclerosis
26
Q

Do we do other investigations (thatn normal histology) in a diabetic person presenting with neuropathy?

A

Yes, we DO.

  • immunofluorescence and electron microscopy
  • this is to exclude another pathology, e.g. antigen-antibody mediated glomerular disease
27
Q

What are the histological features of renal amyloidosis?

A

deposition of abnormal proteins in the kidney (and other organs)

Congo Red staining used to identify the amyloid

28
Q

Crescents

  • what they are
  • what do they mean?
A

Crescents:

  • proliferating epithelial cells -> occur with any injury that breaks capillary wall
  • crescentic glomerulonephritis = rapidly progressive renal disease
29
Q

What is this?

A

Crescenting glomerulonephritis

*proliferation of the cells -> occupy the space in the Bowman’s capsule (no space between the membrane and capillaries) + compression on the capillary tufts

30
Q

What do crescents may lead to?

A

Necrosis and destruction of the glomerulus -> as it is compressing on capillary tufts