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Urinary System > Glomerular Pathology and Clinical Presentations of Kidney Disease > Flashcards

Glomerular Pathology and Clinical Presentations of Kidney Disease Flashcards

1
Q

What are the 4 renal cortical ‘compartments’?

A

Glomerular
Tubular
Interstitial
Vascular

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2
Q

What are the 3 parts of the filtering mechanism?

A

Podocytes
Basement membrane
Endothelium
(Pathology can occur in any one of these)

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3
Q

What are the effects if the filter gets blocked?

A

Decreased GFR

Renal failure

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4
Q

What is nephrotic syndrome?

A

Loss of significant amounts of protein
(Mainly albumin)
Decreased oncotic pressure - oedema

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5
Q

What is nephritic syndrome?

A

Blockage of the glomerulus
Decreased GFR - AKI
Go into renal failure
Often haematuria and hypertension

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6
Q

If a patient presents with nephrotic syndrome, what is the likely site of injury?

A 
Podocyte layer 
(Subepithelial)
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7
Q

What are the common primary causes of nephrotic syndrome?

A

Minimal change glomerulonephritis
Focal segmental glomerulosclerosis (FSGS)
Membranous glomerulonephritis

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8
Q

What are the common secondary causes of nephrotic syndrome?

A

Diabetes mellitus

Amyloidosis

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9
Q

Describe minimal change glomerulonephritis

A 
Childhood/adolescence 
Incidence reduces with increasing age 
Heavy proteinuria/nephrotic syndrome 
Responds to steroids 
May recur 
Usually no progression to renal failure 
Glomerulus looks normal under a microscope - need electron
An unknown circulating factor damages the podocytes
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10
Q

Describe FSGS

A 
Nephrotic 
Glomerulosclerosis (scarred) 
Adults
Less responsive to steroids 
Circulating factor damages podocytes 
Progressive to renal failure - dialysis needed
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11
Q

Describe membranous glomerulonephritis

A

Commonest cause of nephrotic syndrome in adults
Rule of thirds:
1/3 get better
1/3 stay the same
1/3 go onto end stage renal failure
Immune complex deposited - antigen attaches to podocytes then lots of IgG binds
Probably autoimmune but may be secondary

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12
Q

Describe the long term effects of diabetes mellitus on the kidneys

A

Kidneys get more and more leaky - progressive renal failure
Mesangial sclerosis - nodules that are easy to pick up histologically
Basement membrane thickening

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13
Q

Describe IgA nephropathy

A 
Commonest glomerulonephritis 
Can occur at any age 
Classically presents with haematuria 
Relationship with mucosal infections 
Variable histological features and course
\+/- proteinuria 
A significant proportion progress to renal failure 
No effective treatment
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14
Q

What are the 2 extremes of hereditary nephropathies?

A

Thin GBM nephropathy and benign familial nephropathy
To
Alport syndrome

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15
Q

Describe thin GBM nephropathy

A

Isolated haematuria
Thin GBM
Benign course

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16
Q

Describe Alport syndrome

A 
X linked 
Abnormal collage IV 
Associated with deafness
Abnormal appearing GBM 
Progresses to renal failure 
'Basket weaving' abnormally split
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17
Q

Describe Goodpasture syndrome

A

Anti GBM disease
Relatively uncommon but clinically important
Rapidly progressive - acute onset of severe nephritic syndrome
Difficult to reverse
Association with pulmonary haemorrhage (high BP)
Autoantibody to collage IV in BM

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18
Q

What is the treatment for Goodpasture syndrome?

A 
Immunosuppression 
Plasmaphoresis (give donor plasma to get rid of the autoantibody)
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19
Q

Describe vasculitis

A

Group of systemic disorders
No immune complex or antibody deposition
Association with anti-neutrophil cytoplasmic antibody (ANCA)
Nephritic presentation
Treatable if caught early
Urgent biopsy

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20
Q

Are kidney diseases painful?

A

Rarely

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21
Q

How do many kidney diseases present?

A

No symptoms

22
Q

What is acidotic breathing?

A

Over-breathing

Trying to compensate for acidosis by blowing off more CO2

23
Q

If patients say they are tired all the time, what investigations should be done?

A

FBC

Kidney function tests

24
Q

What is uraemic syndrome?

A

Haemolytic anaemia
Acute kidney injury
Low platelet count
Very severe

25
Q

How much extra water do you have to retain before getting peripheral oedema?

A

5L

26
Q

What are some consequences of tubular dysfunction?

A

Impaired concentrating ability - increased frequency and nocturia
Acidosis
Glycosuria
Hormonal complications - metabolic bone disease because cannot activates vit D, anaemia due to lack of EPO and hypertension due to increased renin

27
Q

Why do we usually urinate less frequently at night?

A

Urine is diurnally regulated

Concentrated more at night

28
Q

Why might glycosuria present with tubular dysfunction?

A

Tubular disease causes a lower tubular threshold for glucose
Therefore may excrete glucose even when plasma glucose levels are normal

29
Q

Who should be screened for kidney disease?

A 
Hypertension 
Heart disease
Diabetes
Urinary tract obstruction 
Systemic disease (myeloma, lupus etc)
30
Q

Give some causes of microscopic haematuria

A 
UTIs
Polycystic kidneys 
Renal stones
Renal/bladder tumours 
Arteriovenous malformations 
Kidney/glomerular disease
31
Q

What colour will blood be in from glomerular disease?

A

Brown/smoky in colour

32
Q

Are clots in the blood in urine likely if from the kidneys?

A

No

33
Q

Describe the blood in urine from glomerular disease

A

Brown/smoky in colour
Blood throughout stream
Painless
Clots are very unusual

34
Q

Give some other causes of discoloured urine (brownish)

A

Haemoglobinuria
Myoglobinuria
Consumption of food dyes

35
Q

What is the commonest glomerular cause of haematuria?

A

IgA nephropathy

36
Q

What are red cell casts?

A

Binding of RBCs to a tubular protein that is always present in the urine

37
Q

Why are there often dysmorphic RBCs in the blood?

A

Squeezed through the filtration barrier

38
Q

What does urine with protein in it look it?

A

Frothy

39
Q

Why are people with proteinuria more susceptible to infections?

A

Loss of immunoglobulins

40
Q

Why are people with proteinuria in a pro-thrombotic state?

A

Increased risk of clotting due to imbalance of regulators of coagulation cascade

41
Q

What is the classic triad of findings with nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia
Oedema

42
Q

Why might you get hyperlipidaemia with nephrotic syndrome?

A

Disturbances to liver function

43
Q

What extra-urinary signs suggest nephrotic syndrome?

A

Muehrcke’s bands - horizontal lines across the nails
Xanthelasma
Fat bodies in urine

44
Q

Describe the manifestation of nephritic syndrome

A 
Rapid onset 
Oliguria 
Hypertension 
Generalised oedema 
Haematuria 
Normal serum albumin 
Variable renal impairment 
Some proteinuria
45
Q

What is required for a diagnosis of a nephritic syndrome?

A

Renal biopsy

46
Q

How do nephritic and nephrotic syndromes different?

A 
Nephrotic:
More gradual onset 
More oedema 
Normal BP (raised in nephritic) 
Normal/low JVP 
More proteinuria 
Less haematuria 
Red cell casts usually absent 
Lower serum albumin
47
Q

What is rapidly progressive glomerulonephritis?

A

Glomerular injury so severe that renal function deteriorates over days
May present as uraemic emergency
Associated with crescenteric glomerulonephritis
Antineutrophil cytoplasmic antibodies
Anti GBM antibodies
Often associated with systemic vasculitis

48
Q

How is the glomerulus damaged in vasculitis?

A

‘Blown apart’ by inflammation in the blood vessels
Fibrin leaks out
Profound effect on filtration and tubular function

49
Q

What are the pulmonary manifestations of vasculitis?

A

Opacities

Cavitation lesions

50
Q

With CKD, under what eGFR do you have to be before symptoms occur?

A

< 30 ml/min

51
Q

At what eGFR would we start patients on dialysis?

A

8 - 10 ml/min

52
Q

Give some of the many symptoms of CKD

A 
Tired/lethargic
Breathlessness
Nausea/vomiting
Aches and pains
Sleep reversal 
Nocturia 
Restless legs 
Itching
Chest pains 
Seizures and coma

Urinary System (14 decks)

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