Glomerular Diseases Flashcards

1
Q

What sturctures could be damaged in glomerulonephritis?

A

Capillary endothelium
Glomerular basement membrane
Mesangial cells
Podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What changes can occur in glomerulonephritis?

A

Narrowed capillary lumen
Fusion of foot processes (podocytes)
Increased number of mesangial cells
Subepithelial immune complexes (“humps”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 5 different clinical presentations of GN?

A
  • Asymptomatic proteinurea / haematuria
  • Chronic glomerulonephritis
  • Acute glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Nephrotic syndrome

Most of the diseases can present in more than one of these ways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the difference between nephrotic and nephritic syndromes?

A

Nephrotic - podocytes damage leading to glomerulus charge -barrier disruption + massive proteinurea and oedema

Nephritic - Inflammation disrupting the glomerular basement membrane. It presents with haematuria (coco-cola coloured urine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do you define nephrotic syndrome?

A

Triad of:
Proteinuria
Hypoalbuminaemia
Oedema

Usually accompanied by high cholesterol

BP often normal (but can be high or low)
Creatinine may be normal
Proteinuria > 350mg/mmol alone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are common causes of nephrotic syndrome?

A

Primary:
Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis (FSGS)

Secondary:
Diabetes
SLE
Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do you manage nephrotic syndrome?

A

Oedema:

  • Diuretics, need large dose and may need to be i.v. if gut oedema
  • Salt and fluid restriction

ACE-inhibitor
-anti-proteinuric

Hypercholestrolaemia
- Statin if need be but not always

Treat underlying condition / cause of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you define nephritic syndrome?

A

Triad of:
Haematuria
Reduction on GFR
Hypertension

Other features

  • Proteinuria - less than nephrotic
  • Disruption of the endothelium results in inflammatory response and damage to the glomerulus
  • Onset may be acute or rapidly progressive
  • Rapidly progressive GN is a severe nephritic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some common causes of nephritic syndrome?

A
Anti-GBM disease (goodpasture’s)
ANCA-associated vasculitis 
IgA / Henoch-Schonlein purpura
Post-infectious
Lupus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you manage nephritic syndrome?

A

BP control / reduction of proteinuria

  • ACE
  • Salt

Treatment of oedema

Disease specific treatments
-Generally immunosuppressants

CVS risk management
-Stop smoking, statin ect..

Dialysis (short-term)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is ANCA-associated vasculitis?

A

Granulomatosis with polyangiitis (Wegener’s) and microscopic polyangiitis

Affect small arterioles

Often kidneys and lungs
‘Pulmonary-renal syndrome’

Often systemic symptoms - fatigue, arthralgia, myalgia, weight loss

No immune deposits in kidney - circulating antibodies to white cells. Endothelial damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is anti-GBM disease (Goodpasture’s)?

A

Caused by antibodies to a3 chain of Collage IV in GBM or (but less likely as heard to reach) alveolar basement membrane.

Pulmonary haemorrhage likely- especially if pre existing damage to endothelium (smokers, infection..)

Always cases rapidly progressing glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is systemic lupus erythematosus (SLE)?

A

Auto-immune systemic disease that can affect multiple systems.

Has many different patterns of renal disease
so it can cause nephritic and nephrotic syndrome

Prognosis depends on type of lesion, activity n amount fo kidney involves.

Treatment varies according to pattern of lupus nephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is diabetic Nephropathy?

A

Commonest cause of end stage renal disease.

30-40% of all types of diabetes eventually get ESRD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What pathological changes occur in diabetic nephropathy?

A
  1. Hyperfiltration / capillary hypertension - early, related by hyperglycaemia, glomerular hypertension and increase GFR.
  2. Glomerular basement membrane thickening
  3. Mesangial expansion
  4. Podocyte injury
  5. Glomerular sclerosis / arteriosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How nephron change in DM?

A

Afferent vasodilation and efferent vasoconstriction.

Afferent vasoconstriction:

  • Hyperglycaemia
  • High blood amino acid levels
  • Low NaCl delivery to the macula dense

Also:
Increased NaCl and glucose filtration and reabsorption. (So decreased distal delivery of NaCl)

Efferent vasodilation:
-High local angiotensin II levels.

17
Q

How doe GBM change in DN?

A

Damage to podocytes

Thickened GBM increases pore size

High intraglomerular pressure

Mesangial expansion
More Wilson nodules

18
Q

What are the clinical signs of diabetic nephropathy in the 1st stage (hyper filtration and hypertrophy)?

A

Increased GFR

Normal histology.

19
Q

What are the clinical signs of diabetic nephropathy in the latent stage?

A

Normal albuminurea

GBM thickening and mesangial expansion

20
Q

What are the clinical signs of diabetic nephropathy in the 3rd stage (Microalbuminuria)?

A

Variable mesangial expansion / sclerosis

Increased GBM thickening

Podocyte changes

GFR normal

21
Q

What are the clinical signs of diabetic nephropathy in the 4th stage (Overt proteinuria)?

A

Diffuse glomerular histopathological changes

Systemic hypertension

Falling GFR

Then end stage renal disease

22
Q

How long does it take to develop ESRD?

A

About 20yrs - but not decreasing and less people get to the end.

23
Q

What is microalbuminuria?

A

First clinical sign

GBM thickening and mesangial expansion

Albuminuria
30-300mg/day
‘Albustix’ -used to measure albumin.

At this stage, it is potentially reversible.

24
Q

What is overt proteinuria?

A

Proteinuria over 30mg/mmol Cr detectable on a dipstick.

It was previously associated with ESRD in 3-7years but prognosis is improving lots.

GFR normal then gradually drops.

Mesangial expansion and sclerosis means there is reduced surface area for filtration

Worsening systemic hypertension

Microvascular changes (hyalinosis of arterioles) causes tissue ichaemia.

25
Q

What is the significance of overly proteinuria?

A

Normal GFR and proteinuria < 100mg/mmol = mild kidney disease EXCEPT in diabetes.

Average decline in GFR 12mls/min/yr so most patients reach ESRD in 3-7 years.(But improving..)

26
Q

What are the risk factors for DN?

A
Genetic susceptibility 
Race - Caucasians less likely than south East Asians, Mexicans and blacks 
Hypertension 
Hyperglycaemia 
High level of hyperfiltrtion 
Increasing age
Duration if diabetes 
Smoking
27
Q

How can you prevent diabetic nephropathy?

A

Tight blood glucose control

Tight blood pressure control

28
Q

How do you tightly control glycaemia?

A

Multiple injections or insulin pumps - near normal blood glucose

29
Q

How do you manage microalbuminuria and proteinuria?

A

Inhibitions of RAAS
Tight blood pressure control
Statin therapy
CV

30
Q

Why does RAAS blockage work?

A

It reducesglomerular hyper filtration - efferent > afferent arterioles.

It has anti-proteinuric effect more than just tightly controlling blood pressure.

By reducing proteinuria, it slows the progression at stages 2-4of diabetic nephropathy,

31
Q

What does angiotensin II do?

A

Released following renin release.

Leads to:

  • Increased glomerular permeability to proteins
  • Mesangial cell proliferation
  • Increased mesangial matrix
  • Efferent glomerular constriction -increased glomerular pressure
32
Q

WHy SGLT 2 inhibition work?

A

Because it would help to decrease the absorption fo glucose in the PCT so that more Na” is delivered to the macula dense and glycosuria occurs. This will then cause afferent arteriole constriction

33
Q

Why do children not get diabetic nephropathy?

A

Takes 15 years to develop DN so, are adults when this occurs.