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Sem 3: Urinary > 8a.) Glomerular Pathology > Flashcards

8a.) Glomerular Pathology Flashcards

1
Q

Define glomerulonephritis

A

Any condition associated with inflammation in the glomerular tuft

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2
Q

Define glomerulosclerosis

A

Segmental or global capillary collapse- it is assumed there is little or no filtration across the sclerotic area

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3
Q

Define what we mean when we tlak about proliferative glomerular pathology

A

An increased number of cells in glomerulus; these can be proliferating glomerular cells or infiltrating circulating inflammatory cells

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4
Q

Define what is meant by membranous changes of glomerulus

A

Thickening of glomerular capillary wall

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5
Q

Define what is meant by global changes to glomerulus

A

Involves the entire glomerular tuft

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6
Q

Define what is meant by segmental changes to the glomerulus

A

Involves part of the glomerular tuft

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7
Q

Define what is meant by diffuse changes to glomerulus

A

Involves more than 50% of glomeruli on light microscopy

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8
Q

Define what is meant by focal changes of glomerulus

A

Involves less than 50% of glomeruli on light microscopy

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9
Q

Describe the difference between primary and secondary glomerular disease

A
  • Primary: only kidney is affected e.g. minimal change glomerulonephritis
  • Secondary: disease process affects other organs as well as the kidney e.g. diabetes
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10
Q

We can classify glomerular disease according to what 3 things?

Which of these is a diagnosis?

A
  • Clinical syndrome produced e.g. nephrotic
  • Histopathological appearance e.g. minimcal change
  • Underlying disease e.g. lupus

Only ‘underlying disease’ serves as a diagnosis; however, if the aetiology is unknown the histopathological descripton can be used as a diagnosis e.g. minimal change change glomerulonephritis

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11
Q

What are the 4 structures in the glomerulus that can get damaged in glomerular disease?

A
  • Capillary endothelium
  • Glomerular basement membrane
  • Podocytes
  • Mesangial cells
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12
Q

Clarify the difference between:

  • Focal and segmental glomerular disease
  • Diffuse and global glomerular disease
A
  • Focal= affects some of glomeruli
  • Segmental= affects part of glomerulus
  • Diffuse= affects all of glomeruli
  • Global= affects whole glomerulus
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13
Q

What part of glomerulus is damaged in nephrotic syndrome?

State the triad of symptoms seen in nephrotic syndrome and explain why they occur

A
  • Podocyte damage which leads to abnormal size of filtration slits

Triad of symptoms:

  • Proteinuria >350mg/mmol (or 3.5g in 24hr)
  • Hypoalbuminaemia
  • Oedema
  • Usually accompanied by hyperlipidaemia

Proteins can leak out of glomerulus due to abnoral/increased size of filtration slits (caused by podocyte damage) which leads to protein in urine and a lack of albumin in blood which then decreases oncotic force in capillaries leading to oedema

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14
Q

Alongside the usual triad of symptoms that constitutes nephrotic syndrome; state 3 other features you often see in nephrotic syndrome- think about:

  • Lipidaemia
  • Blood pressure
  • Creatinine
A
  • Hyperlipidaemia: thought that as liver tries to compensate for lost albumin by synthesising more it also increases synthesis of lipids
  • Blood pressure often normal (can be low or high)
  • Creatinine often normal (indicating GFR normal)
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15
Q

In neprhotic syndrome, plasma is lost to the interstitium due to reduced oncotic pressure in capillaries; this can cause a decrease in blodo volume and hence blood pressure which activates RAAS. Explain why RAAS doesn’t work effectively in neprhotic syndrome

A
  • RAAS increases tubular Na+ and therefore water retention
  • However, since there is hypoalbuminaemia and a reduced oncotic force in capillaries the extra fluid that has been retained doesn’t stay in plasma it moves into interstitium
  • This further worsens oedema and doesn’t significantly change blood pressure

JUST MAKE NOTE that BP often normal in nephrotic syndrome

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16
Q

Nephrotic syndrome can be caused by 3 primary renal diseases and 3 secondary renal diseases; state these

A

Primary

  • Minimal change disease
  • Membranous glomerulonephropathy
  • Focal segmental glomerulosclerosis

Secondary

  • Diabetes
  • Systemic lupus erythematosus
  • Renal amyloidosis
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17
Q

Describe how you would manage nephrotic syndrome, think about each of the symptoms and their management to help

A
  • Oedema:
    • Diuretics
    • Salt & fluid retention
  • ACE-inhibitor (antiproteinuric)
  • Treat underlying condition eg. steroids for minimal change disease
  • Hypercholestrolaemia: monitor
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18
Q

When must you exhibit caution when using an ACE inhibitor for neprhotic syndrome?

A

If individual is intravascularly deplete or renal function deteriorating acutely

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19
Q

If we think of the glomerulus as a filter, what two things can go wrong?

A
  • Filter can leak -> nephrotic & nephritic syndrome can lead to proteinuria, haematuria or both
  • Filter can block -> renal failure, decrease GFR
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20
Q

In terms of the glomerulus, what do we mean by:

a. ) subepithelial injury
b. ) subendothelial injury

A
  • Subepithelial: podocyte injury
  • Subendothelial: endothelium damage
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21
Q

Are high concentrations of albumin toxic to nephron?

A

Yes, high concentrations of albumin are toxic to nephron; it can cause acute and chronic inflammation which can lead to fibrosis and a consequent loss of nephrons leading to CKD

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22
Q

Describe minimal change nephropathy, include:

  • What part of glomerular filtration barrier is damaged and what causes damage
  • What syndrome it causes
  • Who it is commonly found in
  • Histological changes
  • How it is treated
  • Risk of progression to renal failure
A
  • Podoctyes damage- think due to uknown circulating factor that damages podocytes- no immune complex deposition
  • Neprhotic syndrome
  • Children & adolescents- often associated with atophy and following URT infection
  • No changes seen in light microscopy (but can see changes in electron microscopy)
  • Steroids
  • Usually no progression to renal failure
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23
Q

Describe focal segmental glomerulosclerosis, include:

  • What part of glomerular filtration barrier is damaged and what causes damage
  • What syndrome it causes
  • Who it is commonly found in
  • Histological changes
  • How it is treated
  • Risk of progression to renal failure
A
  • Podocyte damage- think there is a circulating factor that damages podocytes but scars also contain immunoglobulins. Basically scarring of glomeruli filtration membrane
  • Nephrotic
  • Adults
  • Glomerulosclerosis (focal and segmental scarrring seen)
  • Some response to steroids
  • Potential to progress to renal failure
24
Q

Describe membranous nephropathy, include:

  • What part of glomerular filtration barrier is damaged and what causes damage
  • What syndrome it causes
  • Who it is commonly found in
  • Histological changes
  • How it is treated
  • Risk of progression to renal failure
A
  • GBM becomes inflammed and damaged (podocytes also damaged) increasing permeability of GBM. Autoantibodies produced and form immune complexes which can get stuck in glomerulus. Thicker GBM and damage to podocytes
  • Nephrotic
  • Adults
  • Subepithelial immmune deposits activate complement system; over time thicker glomerular basement membrane develops
  • Treat underlying disease if secondary. Some respond to steroids
  • Some develop end stage renal disease
25
Which part of glomerular filtration barrier is damaged in neprhitic syndrome? What is the triad of symptoms?
Inflammation in glomerulus which causes damage to endothelium (leading to heamaturia) _Triad of symptoms:_ * Haematuria * Reduction in GFR * Hypertension
26
Alongside usual symptoms what other symptoms may someone with nephritic syndrome have?
* Oligouria * Azotemia (high levels of nitrogen-containing compounds in blood e.g. urea and creatinine) * Sometimes proteinuria * Erythrocyte casts
27
Explain why GFR decreases in nephritic syndrome
Inflammation causes damage to glomeruli which results in decline in overall filtration rate. The reduction in GFR reduce capacity for urine formation and hence is what causes oliguria and axzotemia. It also means kidneys cannot properly control BP leadign to hypertension
28
Explain why you have high BP in nephritic syndrome
GFR decreased hence kidneys ability to regulate BP decreased
29
State some common causes of nephritic syndrome
* Acute proliferative glomerularnephritis * IgA Nephropathy * Anti- GM disease/Goodpasture syndrome * Rapidy progressive glomerular nephritis * Alport syndrome * Lupus nephritis
30
Describe antiglomerular basement membrane disease (Goodpasture's syndrome), include: * What it is * What it causes in glomerulus and lung
* Antibodies against type 4 collagen found in aveolar basement membrane in lung and glomerular basement membrane in kidney * Bind to tissues and cause inflammation. In kidneys leads to rapidly progressing glomerular nephritis and in lungs can caue pulmonary haemorrhage. Can also cause vasulitis
31
Describe the management of nephritic syndrome, think about each of the symptoms to help
* Hypertension: * ACE inhibitors * Salt restriction * Treat underlying disease * Cardiovascular risk management * Stop smoking * Statins * Dialysis if GFR reduced massively
32
What is the most commonest cause of ESRD?
**Diabetic nephropathy** Accounts for 30-40% of ESRD Between 25-50% of diabetics develop diabetic nephropathy
33
State the 5 pathological changes that occur in diabetic nephropathy
* Hyperfiltration * Glomerular basement membrane thickening * Mesangial expansion * Podocyte injury * Glomerular sclerosis/arteriosclerosis
34
State/describe the 5 stages of diabetic nephropathy
1. **Hypefiltration & hypertrophy**- increase GFR 2. **Latent stage**: GBM thickening and mesangial expansion 3. **Microalbuminuria**: small amount of albumin detected in urine (not detected on conventional dipstick), further increase in GBM thickening and mesangial expansion, podoyte changes 4. **Overt proteinuria**: lots of albumin in urine/can detect on conventional dipstick, diffuse glomerular histopathological changes, falling GFR 5. **ESRD**
35
What histopathological changes are seen in overt diabetic nephropathy? (3)
* Kimmelstiel-WIlson nodules * Glomerulosclerosis * Hyalinisation of arterioles
36
What are these and what disease are they specific to?
37
Microalbuminuria can be measured using albustixs; is micoralbuminuria in diabetic nephropathy reversibe?
Yes, potentially reversible
38
Is overt proteinuria in diabetic nephropathy reversible?
Not reversible but it's progression can be slowed with treatment
39
Roughly, how long after being diagnosed with overt proteinuria do diabetic patients reach ESRD?
3-7 years
40
State some risk factors for developing diabetic nephropathy
* Genetic susceptibility * Race * Hypertension * Hyperglycaemia * Increasing age * Smoking * Duration of diabetes
41
State two primary prevention methods to prevent diabetic nephropathy
* Tight blood glucose control * Tigh blood pressure control
42
Explain the benefits of tight glycaemic control in regards to diabetic nephropathy
* Can reverse initial hyperfiltration and delay microalbuminuria * Can reduce microalbuminuria over 2 years NOTE: it doesn't really help diabetic nephropathy once you have overt proteinuria
43
Describe how we canmanage microalbuminuria and overt proteinuria in diabetic nephropathy
* Inhibition of RAAS * Tigh blood pressure control * Statin therapy * Cardiovascular risk management e.g. exercise, diet, stop smoking * Tight blood glucose control (does not affect progression once overt proteinuria develops)
44
Explain why we use drugs that inhibit RAAS to treat diabetic nephropathy
Overall help to reduce hyperfiltration by: * Keeps efferent arteriole \> afferent arteriole * Anti-proteinuric effect * Reduce BP
45
What is systemic lupus erythematous? Explain how it can cause nephritic and neprhotic syndrome State some other symptoms someone with lupus may present with
* Chronic condition where body produces autoantibodies that attack many different systems/parts of body * Autoantibodies attack glomeruli filtration membrane-which part they attack and the extent to which they attack it can cause neprhitc or nephrotic syndrome. Different classes of SLE nephritis which are treated differently * Other symptoms: * Butterfly rash * Headaches * Malaise * Joint pain * Mouth ulcers * Many more
46
State some common causes of nephritic syndrome
* Anti-GBM disease (Goodpasture's) * ANCA-associated vasculitis * IGA Nephropathy\* * Post infectious\* * Systemic Lupus Erythematosus\* *\*= associated with immune disease*
47
What is ANCA-associated vasculitis? Explain how it causes nephritic syndrome What other symptoms might someone present with?
* Inflammation of blood vessels due to autoantibodies * **ANCA** (anti-neutrophilic cytoplasmic autoantibodies) a**ttack/attach to neutrophils and then cause the neutrophils to attack small blood vessels in body**- in kidney this can lead to nephritic syndrome * Other symptoms (as can affect anywhere): * Skin rash: if affects vessels in skin * Fatigue, malaise, myalgia, weight loss, night sweats * Lungs: cough up blood * Eyes: blurred vision
48
Are there any immune deposits in the kidney in ANCA-vasculitis?
No- damage done by circulating autoantibodies
49
What is Anti-GBM disease (Goodpasture's disease)? Explain how it causes rapidly glomerulonephritis (often occurs too quick for nephritic syndrome) What other organs it commonly affects?
* Autoantibodies to the a3-chain of type IV collagen in glomerular basement membrane. Autoantibodies attach to basement membrane attracking WBCs which then cause damage to endothelium * Autoantibodies can also attach to a3-chain of type IV collagen in alveolar basement membrane so 50% present with lung issues e.g. SOB, haemoptysis etc...
50
Describe how post-infectious acute glomerulonephritis or rapidly progressive glomerulonephritis can form
Immune complexes, which have formed in repsonse to infection elsewhere in body, become trapped in kidneys when kidneys are filtering the blood leading to inflammation of glomeruli
51
What is IGA nephropathy (Berger disease)? Explain how it can lead to nephritic syndrome What will you in kidney biopsy? Can they have a kidney transplant?
* IGA usually attaches itself to foregin particles in body and activates immune system. In IGA nepthropathy a defective form of IGA attaches itself to another IGA molecule, instead of an infection, forming an immune complex. Immun complex gets trapped in kidneys and then activates immune system to attack glomeruli and damage filtration barrier * Stain IGA fluroscent dye can see * Can have transplant but disease will come back and attack other kidney *
52
What is Alport syndrome? How can it lead to nephritis?
* Mutation in collagen that is found in basement membrane of glomerular filtration barrier- defective barrier allows blood cells to pass through
53
What is renal amyloidosis? How can it lead to nephrotic syndrome?
* Blood illness in which pieces of immunoglobulins bind together to form M protein * M protein gets stuck in glomerulus and stops it acting efficiently as filtration barrier, allows proteins through
54
Outline the potential pathophysiology of diabetic neprhopathy
55
State some causes of: * Nephritic syndrome (acute or chronic glomerulonephritis) * Rapidly progessive glomerulonephritis * Nephrotic syndrome
* Nephritic syndrome: IGA neprhopathy, SLE, post-infectious, ANCA-vasculitis * Rapidly progressive glomerulonephritis: ANCA-vasculitis, Goodpastures (anti-AGM disease), post infectious, SLE * Nephrotic: minimal change, FSGS, membranous,SLE
56
What does anti-GBM disease always lead to?
Rapidly progressive glomerulonephritis

Sem 3: Urinary (21 decks)

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