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PATH30001 - Mechanisms of Disease > Lecture 18 - Renal Pathology 1 > Flashcards

Lecture 18 - Renal Pathology 1 Flashcards

1
Q

Give an overview of the structure of the kidney

A
  • Two per person
  • 150g each
  • Renal artery & vein
  • Ureters
  • Cortex & medulla
  • Renal pyramids
  • Ureteric pelvis
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2
Q

Kidneys & hormones?

A

The kidney makes hormones:
• Renin
• Erythropoietin

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3
Q

What are some general functions of the kidneys?

A
  • Excretion of metabolites & waste
  • Na+ and H20 balance
  • Maintenance of pH
  • Hormone production
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4
Q

What are the ‘four components’ of the kidney?

A

Glomeruli
Tubules
Interstitium
Blood vessels

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5
Q

Describe the anatomy of the glomerulus

How many per adult?

A

Normal adult: 1x10^6

  • Cluster of specialised capillary loops
  • Afferent & efferent arteriole
  • Fenestrated endothelium
  • Specialised basement membrane
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6
Q

Describe basic urine formation

A
  1. Filtration
    Water and solutes pass through fenestrated wall into urinary space
2. Reabsorption
 • Occurs along the tubules
 • PCT: bulk reabsorption
 • Loop of Henle: concentration of urine
 • DCT: fine tuning of urine composition
 • Collecting duct: water reabsorption
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7
Q

What is the metabolic demand of the kidney tubule cells?

A
  • Very high demand

* Due to active transport occurring along the tubules

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8
Q

What is the tubulo-interstitium?

A

Interstitium + kidney tubules

• The function of these two elements is inseparable

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9
Q

What is meant by acute renal disease?

A
  • Quick onset
  • Reversible element to abnormalities

NB Some acute renal injury may be reversible

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10
Q

List the clinical syndromes of renal disease

A
  • Acute renal failure
  • Nephrotic syndrome
  • Nephritic syndrome
  • Gross / macroscopic haematuria
  • Microscopic haematuria
  • Asymptomatic proteinuria
  • Chronic renal failure
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11
Q

What is GFR?

A

Glomerular filtration rate

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12
Q

Describe acute renal failure

What is the aetiology?

A

NB Not a term for general acute renal abnormality!

  • Acute reduction in Glomerular filtration rate (GFR)
  • Reflected as reduced creatinine clearance
  • Increased serum creatinine

3 aetiological groups:

  1. Pre-renal
  2. Renal
  3. Post-renal
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13
Q

What is ‘pre-renal’ acute renal failure?

A

Not enough blood getting to the kidney for proper function

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14
Q

What is ‘renal’ acute renal failure?

What is the most common cause of this?

A

Problem with the kidney itself

Causes:
Most common:
 • Acute tubular necrosis
also
 • Acute Glomerulonephritis
 • Acute interstitial nephritis
etc.
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15
Q

What is ‘post-renal’ acute renal failure?

A

Necessary urinary drainage isn’t happening

```
e.g.
• Ureteric obstruction
calculus in lumen, tumour in wall
• Urethral obstruction
(prostatic enlargement)
~~~

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16
Q

What is nephrotic syndrome?

A

• Leaky glomerulus
• Proteins escape into urine
→ Proteinuria

Features:
 • Oedema (whole body)
- due to reduced plasma oncotic pressure
 • Proteinuria
 • Hypoalbuminaemia
 • Hyperlipidaemia
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17
Q

What are some common causes of proteinuria or nephrotic syndrome?

A
  • Diabetes mellitus
  • Glomerulonephritis
  • Amyloid deposition (Amyloidosis)
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18
Q

Describe Acute tubular necrosis

Reversible / irreversible?

A 
Under-perfusion severe and long enough to cause death of tubular epithelial cells
→
 • Necrosis of tubular epithelial cells
 • Dilation of tubules
 • Tubular casts: sloughing into lumen
 • Oedema in interstitium
 • Glomeruli and vessels preserved

• Reversible

Regeneration
• May take weeks

19
Q

Describe Glomerulonephritis

What are the sequelae?

A 
• Acute injury to the glomerulus
 • Most often immune mediated
 • Deposition of immune complexes in the tuft
→ C' activation
→ Formation of MAC

Rare but important minority due to:
• Direct anti-Glomerular Basement Membrane antibodies

Sequelae:
• Rapid progression w/ crescents
• Reversible
• Slowly progressive to chronic renal failure

20
Q

What are crescents?

In which disease are they observed?

A

Observed in Glomerulonephritis

If severe:
• Clumps of monocytes & epithelial cells accumulate in capillary tufts

Composition:
• Cells
• Fibrin
• Clotted blood

Location:
• Outside the glomerular capillary
• In the urinary space

21
Q

What is a ‘segmental scar’?

A

A slower, less acutely damaging glomerulonephritis

22
Q

Describe acute interstitial nephritis

How does it normally present?

Aetiology?

A

Interstitium and tubules infiltrated by inflammatory cells (eosinophils)

Usually presents as acute renal failure
• +/- blood or protein in urine

Symptoms:
• Fever
• Rash

Aetiology:
• Drug allergy (e.g. antibiotics)

23
Q

Which cells are often seen in the interstitium in acute interstitial nephritis?

A

Eosinophils

24
Q

What are three important causes of acute renal injury?

A
  • Acute tubular necrosis
  • Acute glomerulonephritis
  • Acute interstitial nephritis
25
Q

How much cardiac output do the kidneys receive?

A

20%

26
Q

Why is it significant that the blood in the glomeruli is drained by an arteriole?

A

The efferent arteriole can vasodilator or constrict, controlled very finely the pressure.
GFR can be very finely controlled

27
Q

Where is the urinary space?

A

Inside the Bowman’s capsule

28
Q

What are the mechanisms of control of filtration?

A
  • Foot processes of the podocytes

* Vasodilation & vasoconstriction of the afferent & efferent arterioles to control GFR

29
Q

What type of cells form the tubules?

What is important about them?

A

Specialised epithelium

Very high metabolic demand

30
Q

Where is the basement membrane?

A

Formed on the outside of the endothelium of the glomerulus

31
Q

What is mesangium?

A

= Mesangial cell
Function:
• Phagocytic
• Secrete the amorphous basement membrane-like material known as the mesangial matrix

Contained within the basement membrane

32
Q

Compare acute renal failure and nephrotic syndrome

A

Acute renal failure: not enough blood perfusing

Nephrotic syndrome: leaky basement membrane

33
Q

Explain Starlings forces

A

Plasma osmotic pressure
Plasma hydrostatic pressure

Interstitial osmotic pressure
Interstitial hydrostatic pressure

This maintains volume in capillaries

The proteins in the blood are the main driver of reabsorption of fluid back into the capillaries

34
Q

Is filtration active or passive?

What about reabsorption?

A

Filtration: passive
Reabsorption: active

35
Q

Why do tubular epithelial cells rapidly undergo necrosis

A
  • Highly metabolically active; stuffed with mitochondria

* When ischemic, they rapidly undergo necrosis

36
Q

Is acute tubular necrosis reversible?

A

Yes

After a few weeks on dialysis, the tubules will grow back

37
Q

What is by far the most common cause of acute renal failure?

A

Acute tubular necrosis

38
Q

Where are the foot processes of the podocytes?

A

Wrap around the outside of the glomerular capillaries

39
Q

What gets triggered when immune complexes are deposited in the glomeruli?

A

C’ activation
• Recruitment of inflammatory cells
• MAC formation

40
Q

What is Goodpasture syndrome?

A

A very rare form of Glomerulonephritis

• Caused by antibodies directed against their own basement membrane
• ‘Anti-Basement membrane’ antibodies
→ C’ activation, MAC formation etc. (like in normal GN)

There is the same outcome, but extremely rare

41
Q

Where do crescents form?

A

In the extra-glomerular space (not in the capillary)

42
Q

What can trigger acute glomerulonephritis?

A

Bacterial infection
• Streptococcal infection in throat

NB Antibiotic use could lead to…*

43
Q

What is Bright’s disease?

A

Post-streptococcal acute glomerulonephritis

PATH30001 - Mechanisms of Disease (34 decks)

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