Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis?

A

Immune-mediated disease causing damage to the glomerulus, causing a leak of blood +/- protein into the urine

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2
Q

What causes a) proliferative lesions and RBC in urine and b) non-proliferative lesions and protein in urine?

A

a) damage to the capillary endothelium or mesangial cells b) damage to podocytes

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3
Q

In GN, what may be seen on urine dipstick?

A

Haematuria and/or proteinuria

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4
Q

What does the image show?

A

RBC casts

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5
Q

How might GN present, in terms of direct renal disease?

A

Acute kidney injury- rapidly progressive GN

Hypertension

Nephrotic syndrome

Nephritic syndrome

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6
Q

What is the triad of nephrotic syndrome?

A

Proteinuria, hypoalbuminaemia, oedema

[hypercholesterolaemia is often seen]

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7
Q

What kind of process is nephrotic syndrome indicative of?

A

Non-proliferative

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8
Q

What is a presentation of nephritic syndrome usually indicative of?

A

Nephritic syndrome

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9
Q

What are the main features of nephritic syndrome?

A

Haematuria with RBC casts and dysmorphic RBCs (urine microscopy)

Progressive oliguria and renal failure

Proteinuria

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10
Q

Why are patients with nephrotic syndrome more prone to infection?

A

Loss of immunoglobulins in urine (also immunosuppressive treatments)

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11
Q

Other than infection susceptibility, what are the possible complications of nephrotic syndrome?

A

Thromboembolism (DVT/PE/renal vein thrombosis)

Volume depletion (diuretic use- may lead to pre-renal ARF)

Hyperlipidaemia

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12
Q

How is glomerulonephritis classified?

A

Primary (idiopathic) or secondary (caused by infections, associated with malignancy, part of systemic disease)

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13
Q

What are the general aims of treatment in glomerulonephritis?

A

Reduce proteinuria and preserve long-term kidney function

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14
Q

How is glomerulonephritis managed (non-immunosuppresively)?

A

ACEIs/ARBs

Diuretics

Statins

? Anticoagulation (aspirin/antiplatelets)

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15
Q

What is the target blood pressure in GN a) without proteinuria and b) with proteinuria

A

a) 130/80 b) 120/75

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16
Q

What kinds of immunosuppressive drugs may be used in GN?

A

Corticosteroids

AZT

Cyclophosphamide

Mycophenolate

Calcineurin inhibitors

17
Q

When might plasma exchange (plasmapheresis) be used?

A

Goodpastures disease (to remove the anti basement membrane antibodies)

18
Q

How are nephrotic patients managed?

A

Salt restriction

Diuretics

ACEIs/ARBs

Statins

Treat the underlying cause

19
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change glomerulonephritis (75% of GN in children)

20
Q

What changes are seen in electron microscopy in MCGN?

A

Fusion of podocytes

21
Q

How is MCGN treated and what is the prognosis?

A

Most are steroid responsive (95% go into remission)

Some are steroid-dependent/resistant, or have multiple relapses- second line is cyclophosmamide

Prognosis- about 1% go onto develop ESRF

22
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis

23
Q

What is FSGS sometimes secondary to?

A

vesicouretric reflux, IgA nephropathy, heroin use, HIV, obesity

24
Q

What is the second most common cause of nephrotic syndrome in adults?

A

Membranous nephropathy

25
What is membranous nephropathy associated with? a) drugs b) infection c) systemic disease
a) gold, penicillamine b) HBV, parasites c) maligancy, lupus, RA
26
What changes are seen in renal biopsy of membranous nephropathy, and how does it usually present?
Diffuse thickened basement membrane, sub-epithelial deposits of IgG and C3 Usually nephrotic syndrome
27
What proportion of membranous nephropathy patients will progress to ESRF?
30% within 10 years
28
What is the most common GN in the developed world?
IgA nephropathy
29
How does IgA nephropathy present?
Macro- or micro-haematuria Typical presentation- young male with episodic macroscopic haematuria occurring a few days after URTI
30
What is the systemic manifestation of IgA nephropathy? How does this present?
Henoch-Schonlein purpura Purpuric rash, polyarthritis, abdominal pain
31
How are IgA nephropathy/HSP treated?
BP control ACE inhibitors
32
What is the main classification of rapidly progressive GN?
ANCA -ve: IgA/HSP, SLE, Goodpasture's Disease ANCA +ve: systemic vasculitis e.g. Wegeners, microscopic polyangiitis
33
What is the common biopsy finding in patients with RP-GN?
Glomerular crescents
34
How is RP-GN treated?
Aggressive immunosuppression (steroids and cyclophosmamide) + plasma exchange
35