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PATH30001 - Mechanisms of Disease > Lecture 19 - Renal Pathology 2 > Flashcards

Lecture 19 - Renal Pathology 2 Flashcards

1
Q

What is the connotation of ‘chronic’ renal disease?

A
  • Irreversible

* Long duration

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2
Q

What is the formal definition (in terms of GFR) of chronic renal failure?

A

GFR Less than 15mL / minute

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3
Q

What clinical condition often accompanies chronic renal failure?

A

Hypertension

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4
Q

What is the difficulty with clinical detection of chronic renal injury?

A

There is enormous renal function reserve: the other kidney
• Ability to survive with just one kidney

Thus CRF is often only detected late in the course

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5
Q

What is the macroscopic appearance of a kidney undergoing chronic renal failure?

A

No matter what the cause:

  • Shrunken
  • Scarred, fibrotic
  • Pale (due to loss of glomeruli)
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6
Q

What are the clinical presentations of CRF?

A
  1. Asymptomatic
    • Blood / urine test taken for various reasons
  2. Symptomatic
    • Anaemia
    • Lethargy
    • Anorexia / nausea
3. End stage renal failure
 • Coma
 • Pericarditis
 • Sepsis
 • Neuropathy
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7
Q

How is CRF assessed once it’s diagnosed?

A 
Severity
 • GFR
 • Creatinine clearance
 • Kidney size
 • Haemoglobin (indicator of anaemia)
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8
Q

What are the causes of CRF?

A

2012:
35% Diabetic nephropathy
23% Glomerulonephritis
15% Hypertension

NB 15 years ago, Diabetic nephropathy and GN were in opposite positions

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9
Q

What are the treatment options for CRF?

Which has a better survival rate?

A
  • Transplant
  • Dialysis

Transplant has a 6-fold better survival rate than dialysis

NB There is a selection bias: people who are given transplants are likely to have better outcomes (children)

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10
Q

Describe how Diabetes Mellitus can lead to CRF

A
  • Diabetic glomerulosclerosis / arteriosclerosis
  • Infection → Pyelonephritis
  • Papillary necrosis
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11
Q

What is pyelonephritis?

A

Caused by bacterial infection spread from:
• Urinary tract
• Circulation

Inflammation of kidney

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12
Q

How does DM-glomerular disease present?

A
  • Proteinuria
  • Nephrotic syndrome
  • Deposition of glycosylated proteins in mesangium
  • Slow control of glycaemia & BP
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13
Q

What is a Kimmelstiel-Wilson nodule?

A

Cardinal sign of DM-glomerular disease

• Collagen nodules forms in glomerular capillaries

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14
Q

What are some examples of chronic glomerulonephritis?

What is the commonest form?

A
  • IgA nephropathy
  • FSGS: Focal & Segmental glomerulosclerosis
  • Lupus nephritis

IgA nephropathy is the most common form worldwide

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15
Q

Describe IgA nephropathy

How does it present?

A

Presence of predominantly IgA immune complexes in mesangium

In the past was though to be not so severe, but now is considered to be more severe
Majority of cases progress on to CRF

Presents as:
• Blood in the urine
• CRF

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16
Q

Describe FSGS

How does it present?

A

(Focal and Segmental Glomerulosclerosis)

Causes:
Secondary to:
 • Obestiy
 • Infection
 • Hypertension
'Primary':
 • Circulating toxin that affects podocytes

Presents as:
• Heavy proteinuria
• Clinical nephrotic syndrome

17
Q

Describe Glomerulonephritis in SLE

A

SLE:
• Multi system disease
• Frequent involvement of the kidneys
• Progression various greatly, some progresses to CRF
• Enormous immune complex load in the basement membranes in glomeruli
→ C’ activation; MAC formation

18
Q

Define hypertension, and talk about it as a cause of CRF

A

Hypertension: chronically elevates systemic arterial BP

Nephrosclerosis:
• End result of longstanding HT
• Bilaterally shrunken, granular kidneys
• Larger scars
• Atheroma of larger arteries
• Sclerosis of arterioles
• Scarring of glomeruli and interstitium

19
Q

Describe polycystic kidney disease

A
  • Genetic basis
  • Autosomal dominant
  • Cysts in Liver, Pancreas & Kidneys
  • Small aneurysms in brain
  • Bilaterally huge kidneys
20
Q

Which type of collagen is a major constituent in glomerular basement membranes?

A

Type IV collagen

21
Q

Describe Alport syndrome

How does it present?

A

• Genetic mutation in gene for Type IV collagen
(most X-linked, fewer autosomal)
• Type IV collagen a major constituent in glomerular basement membrane

Presentation:
• Haematuria, not necessarily proteinuria. How bizarre
• Progressing deafness
• Ocular abnormalities

Progression to end stage renal failure

22
Q

Describe Analgesic nephropathy

How does it present?

A 
Longstanding use of 'compound analgesics'
Containing:
 • Phenacetin
 • Caffeine
 • Aspirin
  • Direct toxic effects of phenacetin metabolites
  • & vascular effects
Presentation:
 • Bilaterally shrunken kidneys
 • Papillary necrosis
 • Calcification
 • Deteriation of renal function
 • Possible obstruction of ureter by sloughed off papilla
23
Q

What are the radiological appearances of analgesic nephropathy?

A
  • Swollen cortex
  • Detachment
  • Calcification
  • Undulating outline
24
Q

What is papillary renal necrosis?

A

Necrosis of renal papilla, which are supplied by the vasa recta

Renal papilla:
• Where medullary pyramids empty into minor calyces

25
Q

At what point does CRF present?

A

Once damage is extensive

May take years to get to this point

26
Q

What causes the anaemia of CRF?

A

EPO produced by kidneys

Decreased levels of EPO in body

27
Q

Compare asymptomatic presentation in acute and chronic renal failure

A

Acute: picked up because we notice these things
Chronic: can be asymptomatic, and thus do not get picked up for years

28
Q

Describe what happens to the following parameters in CRF:
• Size of the kidney
• Blood conc. of creatinine

A

Size: Shrinks progressively

When the kidneys are 50% shrunken, creatinine in the blood is not yet all that elevated

90% loss of kidney function: kidneys are tiny
• too late to treat CRF

29
Q

What happens with renin in chronic renal failure?

A

Secretion of Renin
Activation of RAS → elevation of BP
Chronic hypertension is a cause of renal injury

This creates a vicious cycle

30
Q

What is the commonest cause of chronic renal failure in Australia?

A

Diabetes mellitus

31
Q

What is the effect of Diabetes mellitus on immunity?

A

DM decreases neutrophil function

DM patients are more prone to infection

32
Q

Is Alport syndrome X linked or autosomal?

A

Most are X-linked

33
Q

What was so bad about Phenacetin?

A

Caffeine + aspirin

Was supposed to be taken for a headache

The caffeine dependance caused headaches when not having Bex

People took these for everyday
→ Analgesic nephropathy

The compounds damage the medulla of the kidney (where the Loop of Henle dips down)
• Microvasculature affected

34
Q

What is the pathogenesis of analgesic nephropathy?

A

Direct toxic & vascular effects of the analgesic metabolites

35
Q

What is the inheritance of polycytic kidney disease?

A

Autosomal dominant

36
Q

What is the typical pathological feature of DM-glomerular disease?

A

Kimmelstiel-Wilson nodule

PATH30001 - Mechanisms of Disease (34 decks)

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