Session 8: Glomerular Disease - Glomerulonephritis & Diabetes Mellitus Flashcards

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1
Q
A
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2
Q

Give the common histological pathological changes found in glomerulonephritis.

A

Subepithelial immune complexes

Increased number of mesangial cells

Fusion or destruction of podocytes

Narrowed, damaged, or leaky capillaries (endothelial damage)

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3
Q

Four structures of the glomerulus that can be damaged in glomerulonephritis.

A

Capillary endothelium

Glomerular basement membrane (GBM)

Mesangial cells

Podocytes

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4
Q

What is glomerulonephritis (GN)?

A

Inflammation of the glomeruli

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5
Q

Clinical presentation of GN (degrees)

A

Asymptomatic haematuria and/or proteinuria

Chronic GN

Acute GN (Nephritic syndrome)

Rapidly progressive glomerulonephritis (RPGN)

Nephrotic syndrome

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6
Q

Causes of asymptomatic haematuria and/or proteinuria.

A

IgA

SLE

FSGS

etc…

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7
Q

Causes of chronic GN

A

IgA

SLE

Any treated GN

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8
Q

Causes of nephritic syndrome

A

IgA

SLE

ANCA-vasculitis

Anti-GBM

Alport Syndrome

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9
Q

Causes of RPGN

A

ANCA-Vasculitis

Anti-GBM

Post-infectious

SLE

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10
Q

Causes of nephrotic syndrome

A

MCG

FSGS

Membranous glomerulonephritis

SLE

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11
Q

Key differences between nephritic syndrome and nephrotic syndrome.

A

Nephritic:

Inflammation with a triad of haematuria, hypertension and reduced GFR. There is also cola-colored urine and oliguria.

Nephrotic:

Damage to podocytes causing reduction in selectivity of filtration. This leads to a triad of symptoms of proteinuria, hypoalbuminaemia and oedema. You may also see hyperlipidaemia in nephrotic syndrome.

Oedema can occur in both syndromes.

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12
Q

BP and creatinine in nephrotic syndrome.

A

Usually normal.

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13
Q

What is a proteinuria at above 350 mg/mmol called if it is presented without the triad of symptoms seen in nephrotic syndrome?

A

Nephrotic range proteinuria.

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14
Q

Primary causes of nephrotic syndrome.

A

MCG

Membranous glomerulonephritis also called membranous nephropathy also called membranous glomerulonephropathy.

FSGS

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15
Q

Secondary causes of nephrotic syndrome.

A

Diabetes

SLE

Renal amyloidosis

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16
Q

What is the difference between DM and amyloidosis leading to nephrotic syndrome compared to SLE leading to nephrotic syndrome?

A

DM and Amyloidosis solely lead to nephrotic syndrome and glomerulonephritis. They are not classed as GNs.

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17
Q

Managment of nephrotic syndrome.

A

Treating the triad of symptoms.

Oedema by thiazides, loop diuretics (furosemide most commonly) or spironolactone. If this doesn’t work due to the damage of the kidneys salt and fluid restrictions.

ACE-inhibitors

Might give statins for hypercholesterolaemia if there is long-term nephrotic syndrome.

Treating the underlying cause (steroids for MCD e.g.)

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18
Q

Triad of nephritic syndrome.

A

Haematuria

Reduction in GFR (renal impairment/oliguria)

Hypertension

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19
Q

Other clinical features found in nephritic syndrome.

A

Can cause slight proteinuria (Protein+)

The onset may be acute or rapidly progressive (Means it can be Acute GN or RPGN/Crescentic GN)

20
Q

Common causes of nephritic syndrome.

A

Anti-GBM disease (Goodpasture’s)

ANCA-associated vasculitis

IgA nephropathy (Berger’s disease)

Post-infectious associated with immune disease.

SLE

Henoch-Schönlein purpura

21
Q

Management of nephritic syndrome.

A

Blood presssure control by ACE-inhibitors or Angiotensin II receptor antagonists. Salt restriction.

Treatment if oedema arises

Immunosuppressants specific for the underlying disease.

In case of RPGN prednisolon, cyclophosphamide etc.. might be given.

Stop smoking

Dialysis

22
Q

What is ANCA-associated vasculitis?

A

EIther granulomatosis with polyangiitis (Wegener’s) or microscopic polyangiitis.

Affecting small arterioles

23
Q

Why is ANCA-associated vasculitis often called a pulmonary-renal syndrome?

A

Because it commonly affects the kidneys and lungs.

24
Q

Give common systemic symptoms associated with ANCA-associated vasculitis.

A

Fatigue, arthralgia, myalgia and weight loss.

25
Q

How does vasculitis cause renal damage?

A

No immune deposits in the kidneys but rather circulating antibodies to white cells.

Endothelial damage as well.

26
Q

What is anti-GBM caused by?

A

Caused by anti-bodies binding to alpha3 chain of type IV collagen in glomerular basement membrane. This leads to damage to GBM.

27
Q

Why is anti-GBM clinically important?

A

Because if it goes untreated it will always lead to RPGN.

28
Q

Where else might anti-GBM present complications?

A

In the lungs by antibodies binding to alpha3 chains of type 4 collagen in the alveolar basement membrane.

This can lead to pulmonary haemorrhage and often occurs in smokers with pre-existing damage to the alveolar membrane.

29
Q

Common histological presentation of diabetic nephropathy.

A

Kimmelstiel-Wilson nodules (KW)

Thicken GBM.

Mesangial expansion.

30
Q

Why don’t paediatricians see patient’s with diabetic nephropathy?

A

Because children with diabetes will not present with nephropathy until later in life. It takes years for this damage to build up into something noticeable.

31
Q

Is diabetic nephropathy a glomerulonephritis?

A

No it’s not an inflammatory condition.

It is a glomerulopathy.

32
Q

Pathological changes in diabetic nephropathy.

(In rough order)

A

Hyperfiltration and capillary hypertension

GBM thickening

Mesangial expansion

Podocyte injury

Glomerular sclerosis and arteriolosclerosis

33
Q

What causes the hyperfiltration and hypertrophy of the early stages of diabetic nephropathy?

A

Hyperglycaemia and glomerular hypertension.

This leads to an increase in GFR.

34
Q

Clinical signs and symptoms in diabetic nephropathy.

(In rough order)

A

1 - Hyperfiltration and hypertrophy leading to increased GFR.

2 - Latent stage where there will be normal albuminuria and some GBM thickening as well as mesangial expansion.

3 - Some microalbuminaemia (increase). Continued mesangial expansion and some sclerosis. Increased GBM thickening and some changes to podocytes. The GFR returns to normal.

4 - Overt proteinuria with a diffuse glomerular histopathlogical change. Systemic hypertension and a fall in GFR.

5 - ESRD

35
Q

How does GFR change in the different stages of diabetic nephropathy?

A

In 1-2 there is a rise in GFR.

3 - Normal GFR

4-5 Fall in GFR

36
Q

What is the first clinical sign of diabetic nephropathy?

A

Stage three with microalbuminuria.

This is also associated with GBM thickening, mesangial expansion and podocyte changes.

It is important to note that the diabetic nephropathy is still reversible at this stage

37
Q

When is diabetic nephropathy not reversible anymore?

A

When it has reached stage 4 with overt proteinuria.

38
Q

Explain overt proteinuria.

A

Drop in GFR due to mesangial expansion and sclerotic changes in the glomerulus causing reduced surface area for filtration.

Systemic hypertension.

Microvascular changes with hyalinosis of the arterioles that can lead to tissue ischaemia.

Can lead to ESRD within 3-7 years

39
Q

Why is overt proteinuria in diabetes especially important?

A

Because the presentation of Normal/slightly low GFR and proteinuria of <100 mg/mmol only shows mild kidney disease.

This is unless the patient is diabetic. If the patient is diabetic this is much more destructive and can cause ESRD within 3-7 years.

40
Q

Diabetic nephropathy risk factors.

A

Genetic susceptibility (DM typ 1 with 1st degree relatives with DN has an 83% risk of developing it themselves, only 17% risk if no DN of relative)

Ethnicity

Hypertension

Hyperglycaemia

High level of hyperfiltration

Increasing age

Duration of the diabetes

Smoking

41
Q

Primary prevention of diabetic nephropathy.

A

Tight blood glucose control keeping the glucose at <48 mmol/mol

Tight blood pressure control

SGLT-2 inhibitors

Not smoking + statin therapy (more associated with the vascular changes of diabetes)

42
Q

Management of microalbuminuria and overt proteinuria.

A

Inhibition of RAAS

BP control

Statin therapy

Moderate protein intake

43
Q

Explain how inhibition of RAAS can help microalbuminuria and proteinuria.

A

Reduces the glomerular hyperfiltration

The efferent arteriole is more affected.

44
Q

Explain how angiotensin II antagonists can help in microalbuminuria and proteinuria.

A

Angiotensin II leads to increased glomerular permeability to proteins. It also causes mesangial cell proliferation, mesangial matrix proliferation and efferent glomerular constriction.

Antagonising all of this is preferential in diabetic nephropathy.

45
Q

Define glomerulopathy.

A

Pathology to the glomerulus

46
Q

Define glomerulonephritis.

A

Inflammation of the glomerulus

47
Q
A