Glomerular Pathology and Clinical Presentations of Kidney Disease Flashcards Preview

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Flashcards in Glomerular Pathology and Clinical Presentations of Kidney Disease Deck (52)
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1

What are the 4 renal cortical 'compartments'?

Glomerular
Tubular
Interstitial
Vascular

2

What are the 3 parts of the filtering mechanism?

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

3

What are the effects if the filter gets blocked?

Decreased GFR
Renal failure

4

What is nephrotic syndrome?

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

5

What is nephritic syndrome?

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

6

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

Podocyte layer
(Subepithelial)

7

What are the common primary causes of nephrotic syndrome?

Minimal change glomerulonephritis
Focal segmental glomerulosclerosis (FSGS)
Membranous glomerulonephritis

8

What are the common secondary causes of nephrotic syndrome?

Diabetes mellitus
Amyloidosis

9

Describe minimal change glomerulonephritis

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

10

Describe FSGS

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

11

Describe membranous glomerulonephritis

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

12

Describe the long term effects of diabetes mellitus on the kidneys

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

13

Describe IgA nephropathy

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

14

What are the 2 extremes of hereditary nephropathies?

Thin GBM nephropathy and benign familial nephropathy
To
Alport syndrome

15

Describe thin GBM nephropathy

Isolated haematuria
Thin GBM
Benign course

16

Describe Alport syndrome

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

17

Describe Goodpasture syndrome

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

18

What is the treatment for Goodpasture syndrome?

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

19

Describe vasculitis

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

20

Are kidney diseases painful?

Rarely

21

How do many kidney diseases present?

No symptoms

22

What is acidotic breathing?

Over-breathing
Trying to compensate for acidosis by blowing off more CO2

23

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

FBC
Kidney function tests

24

What is uraemic syndrome?

Haemolytic anaemia
Acute kidney injury
Low platelet count
Very severe

25

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

5L

26

What are some consequences of tubular dysfunction?

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

Why do we usually urinate less frequently at night?

Urine is diurnally regulated
Concentrated more at night

28

Why might glycosuria present with tubular dysfunction?

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

29

Who should be screened for kidney disease?

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

30

Give some causes of microscopic haematuria

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