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Renal > Glomerulonephritis > Flashcards

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
Q

What is membranous nephropathy associated with?

a) drugs
b) infection
c) systemic disease

A

a) gold, penicillamine
b) HBV, parasites
c) maligancy, lupus, RA

26
Q

What changes are seen in renal biopsy of membranous nephropathy, and how does it usually present?

A

Diffuse thickened basement membrane, sub-epithelial deposits of IgG and C3

Usually nephrotic syndrome

27
Q

What proportion of membranous nephropathy patients will progress to ESRF?

A

30% within 10 years

28
Q

What is the most common GN in the developed world?

A

IgA nephropathy

29
Q

How does IgA nephropathy present?

A

Macro- or micro-haematuria

Typical presentation- young male with episodic macroscopic haematuria occurring a few days after URTI

30
Q

What is the systemic manifestation of IgA nephropathy? How does this present?

A

Henoch-Schonlein purpura

Purpuric rash, polyarthritis, abdominal pain

31
Q

How are IgA nephropathy/HSP treated?

A

BP control

ACE inhibitors

32
Q

What is the main classification of rapidly progressive GN?

A

ANCA -ve: IgA/HSP, SLE, Goodpasture’s Disease

ANCA +ve: systemic vasculitis e.g. Wegeners, microscopic polyangiitis

33
Q

What is the common biopsy finding in patients with RP-GN?

A

Glomerular crescents

34
Q

How is RP-GN treated?

A

Aggressive immunosuppression (steroids and cyclophosmamide)

+ plasma exchange

35
Q
A

Renal (32 decks)

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