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Clinical Pathology in Action > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

What is the function of the kidney

A
  • Converts 1700 litres of blood per day into about 1litre of urine
  • Excretes the waste products of metabolism
  • Precisely regulates the body’s concentration of water and salt
  • Maintains appropriate acid balance of the plasma
  • Serves as an endocrine organ - produces renin
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2
Q

What is the glomerulus

A
  • A network of tiny blood vessels (capillaries) within the kidney
  • It is a filtering membrane (basement membrane, endothelium and two layers of epithelium including podocytes with pedicels)
  • High permeability for water and small solute
  • Impermeability for protein molecules: glomerular barrier function depending on protein size and charge
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3
Q

What is the histology of the glomerulus

A
  • Network of capillaries
  • The glomerular basement membrane (GBM)
  • Podocytes
  • Mesangial cells
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4
Q

What is the GBM

A

A trilaminar matrix that acts as a filtration barrier formed by the fused basal laminae of endothelial cells and podocytes

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5
Q

What are podocytes

A

These are specialised epithelial cells that have pedicles that interdigitate to form filtration slits that further restricting big molecules from passing through

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6
Q

What are the clinical manifestation of renal diseases

A
  • Acute Nephritic syndrome: Hematuria (blood in urine)
  • Nephrotic syndrome: Heavy proteinuria (protein in urine)
  • Asymptomatic hematuria or proteinuria
  • Acute renal failure
  • Chronic renal failure
  • Urinary tract infection
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7
Q

What is Nephrotic syndrome

A

It is a clinical condition caused by damaged glomeruli. This is specifically when the glomerular capillary wall becomes abnormally permeable, letting proteins leak out of the blood into the urine

Heavy proteinuria (>3.5g/d protein in urine)

  • Hypoalbuminaemia
  • Severe edema
  • Hyperlipidaemia
  • Lipiduria
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8
Q

What is heavy proteinuria in Nephrotic Syndrome

A

> 3.5g/d protein in urine - this is a huge amount

The glomerulus normally keeps large, negatively charged proteins like albumin in the blood stream

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9
Q

What is Hypoalbuminaemia

A
  • Since so much albumin (a major plasma protein) is lost in urine, its level in the blood drops
  • Albumin is crucial for maintaining oncotic pressure - keeps fluid in the blood vessels
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10
Q

How does Hypoalbuminaemia cause severe oedema

A

Low albumin -> Low oncotic pressure -> water leaks out of blood vessels into the tissues -> swelling (oedema), especially in legs, face and abdomen

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11
Q

How does Hypoalbuminemia cause Hyperlipidaemia

A

The liver tries to compensate for the low albumin by increasing production of proteins including lipoproteins

This leads to high cholesterol and triglycerides

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12
Q

How does Hyperlipidaemia cause lipiduria

A

Fat droplets and ‘oval fat bodies’ can be seen in the urine - because of the increased filtration of lipids through the damaged glomeruli

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13
Q

Nephrotic syndrome is caused by primarily:

A
  • Minimal change disease
  • Focal Segmental Glomerulosclerosis
  • Membranous glomerulopathy
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14
Q

Nephrotic syndrome causes secondarily:

A
  • Diabetes Mellitus
  • Amyloidosis
  • Systemic Lupus Erythematosus
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15
Q

What is Minimal Change Disease (MCD)

A
  • Leading cause of nephrotic syndrome in children (ages 2-6)
  • The pedicels are flattened and fused together, seen only in EM, disrupts the filtration barrier allowing protein to leak into the urine
  • Pathogenesis is unknown but possible to be immunologic response to infections
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16
Q

How does MCD look on light microscopy

A

The kidney tissue looks completely normal - there are no inflammatory cells, scarring, or structural damage - hence the name ‘MCD’

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17
Q

How do you treat MCD

A
  • MCD responds extremely well to steroids like prednisone
  • Most children go into remission quickly after starting corticosteroids
  • This rapid steroid response is a hallmark of MCD
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18
Q

What is Membranous Glomerulopathy

A
  • A chronic immune mediated glomerular disease that is the most common cause of nephrotic syndrome
  • It present with massive proteinuria
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19
Q

How does Membranous Glomerulopathy start

A

Immune complexes form and deposit on the sub-epithelial side (just under the podocytes)

These deposits are seen as electron dense in EM

The immune deposits activate complement, leading to podocyte injury and protein leakage

20
Q

What is Primary Membranous Glomerulopathy

A

This is where the body makes autoantibodies against podocyte antigens, especially;

  • PLA2R
  • Thrombospondin Type-1 domain-containing 7A (THSD7A)

These antibodies drive immune complex formation and damage the filtration barrier

21
Q

What is Secondary Membranous Glomerulopathy

A

This is associated with systemic diseases such as:

  • drugs: NSAIDs
  • Malignancy: solid tumours
  • Autoimmune diseases: Systemic Lupus Erythematosus
  • Infections: Hep.B, Hep. C, Malaria
22
Q

What is the pathogenesis of Membranous Glomerulopathy

A

Antigen-antibody mediated disease

Insidious onset - a condition that develops slowly and subtly, with symptoms appearing gradually and not noticed until condition is advanced or serious.

10% progress to chronic disease

40% develop renal insufficiency

23
Q

What is Focal Segmental Glomerulosclerosis (FSGS)

A

FSGS is a pattern of glomerular injury

Focal - Only some of the glomeruli are affected

Segmental - Only part of each affected glomerulus is sclerosed (scarred)

Sclerosis - Hardening/scarring due to the deposition of ECM leading to the loss of filtering capacity

24
Q

What conditions can cause FSGS

A

HIV - Classic cause of collapsing variant of FSGS

Obesity - Causes hyperfiltration and glomerular stress

Hypertension - Chronic high pressure damages glomeruli

Sickle cell anaemia - Ischemic injury and glomerular scarring from sickling of red cells

25
What can cause idiopathic FSGS
Thought to involve a circulating permeability factor that damages the podocytes which leads to proteinuria and then sclerosis
26
What is the adaptive response in glomerular ablation (unilateral renal agenesis)
When there is a loss of nephrons, the remaining glomeruli hyperfilter to compensate Over time, the overwork leads to glomerular injury and sclerosis - an adaptive but harmful response.
27
How does FSGS respond to corticosteroids
Unlike MCD, FSGS does not respond well to steroids Steroid-resistant FSGS is more likely to progress to chronic kidney disease and eventually end-stage renal disease The proteinuria may persist or worsen and patients eventually develop permanent kidney damage, requiring dialysis or transplant
28
What is Diabetic Nephropathy
Leading cause of chronic kidney disease and end-stage renal disease It is a progressive condition that can start of with small structural changes in the kidney and can eventually lead to complete kidney failure
29
What happens in Diabetic Nephropathy
There is specific glomerular damage caused by hyperglycemia in diabetes
30
What is the pathogenesis of Diabetic Nephropathy
Chronic high blood sugar leads to: - Non-enzymatic glycosylation of proteins: forms Advanced Glycation End products (AGEs) - AGEs deposit in the glomerular basement membrane (GBM) and mesangium, damaging them - These AGEs alter protein function, increase oxidative stress, and trigger inflammation
31
How is the GBM biochemically altered
- It becomes thickened, but less effective as a filtration barrier - More permeable to proteins like albumin leading to proteinuria
32
What happens to mesangial cells in the glomerulus
The mesangial cells which support the glomerular capillaries proliferate and produce excess matrix causing: - expansion of the mesangial area - Glomerular sclerosis Overtime this compresses the capillaries, reducing the filtration surface and progressive loss of function
33
What is the progression of damaged mesangial area
1) Hyperfiltration 2) Silent stage - structural changes but no symptoms 3) Microalbuminuria (small protein leak) 4) Proteinuria 5) End-stage renal disease
34
What are the other diabetic effects on the kidneys
- Affects the arterioles - Increased susceptibility to pyelonephritis including papillary necrosis - Variety of tubular lesions
35
How are arterioles affected in diabetic nephropathy
- Diabetes causes hyaline arteriosclerosis - thickening and stiffening of small arteries - leads to ischemia (lack of blood flow) in kidney tissue
36
How does diabetes cause susceptibility to pyelonephritis
Diabetics are more prone to pyelonephritis, especially due to: - Weakened immunity - High glucose in urine (good medium for bacterial growth) Papillary necrosis = death of kidney papillae (tips of renal pyramids) due to poor perfusion
37
How does diabetes cause a variety of tubular lesions
- Thickened tubular basement membrane - Atrophy (shrinking) of tubules - Interstitial fibrosis (scarring between tubules)
38
What is Amyloidosis
It is not one single disease but rather a group of conditions characterised by the abnormal deposition of amyloid proteins in various tissues and organs This leads to organ dysfunction It depends on the type of precursor protein and the underlying condition (chronic inflammation, cancer or genetic causes)
39
What is amyloid
It is a misfolded, insoluble protein that accumulates outside cells, forming fibrils that disrupt normal organ function These proteins are beta-pleated sheets under the microscope
40
What is the primary (AL type) of Amyloidosis
- AL = Amyloid Light chain - Derived from immunoglobulin light chains produced in plasma cell disorders (B cell lymphoma) - Deposits can affect kidneys, heart, nerves and GI tract
41
What is the secondary (AA type) of Amyloidosis
- AA = Amyloid A protein - Occurs in chronic inflammation (TB, rheumatoid arthritis) - The liver produces serum amyloid A (SAA) in response to inflammation and this breaks down and deposits as amyloid - Often affects the kidneys, liver and spleen
42
What is Systemic Lupus Erythematosus (SLE)
SLE is chronic, multisystem autoimmune disease where the immune system attacks the body's own tissues, particularly the nuclear antigens
43
What does SLE affect
- Skin - Joints - Kidneys - Blood - Serosal membranes It has a relapsing-remitting course (it flares up and then it improves)
44
What are the autoantibodies that are present in SLE
- ANA (Antinuclear Antibodies) - Anti-dsDNA (associated with renal disease) - Anti-Smith (Sm) These antibodies form immune complexes that deposit in tissues - triggering inflammation and damage
45
What is the pathogenesis of SLE
Failure of the regulatory mechanism that sustain self tolerance which allows the B cells to make autoantibodies The immune complexes activates complement, recruiting inflammatory cells, leading to tissue injury Autoantibodies form against an array of nuclear and cytoplasmic components of cells and against cell surface antigens Genetic, environmental and hormonal factors contribute
46
What are the clinical manifestations of SLE
- Skin: malar rash, photosensitivity - Joints: arthritis - Kidney: Lupus nephritis - Serosa: Pleuritis, pericarditis - Blood: Anemia, leukopenia
47
How is SLE diagnosed
Based on a combination of clinical features and and immunological markers ANA test is a screening tool, followed by anti-dsDNA and anti-Sm for confirmation

Clinical Pathology in Action (18 decks)

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