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Renal > GN > Flashcards

GN Flashcards

1
Q

Where does HSP appear?

A

Extensor surfaces, buttocks

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2
Q

Nephrotic syndrome

A

Hypoalbuminaemia
Proteinuria >3g/day
Oedema (peripheral, facial)
Hypercholesterolaemia

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3
Q

Nephritic syndrome

A 
Oedema (pulmonary)
AKI
Oliguria
HT
Active urinary sediment (RBCs, granular casts, proteinuria)
- Post strep GN
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4
Q

GN can present in 2 ways:

A

Chronic GN - most common cause of ESRF after diabetes

Acute GN - treatable cause of AKI

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5
Q

How is the glomerulus damaged?

A

Immune mediated with secondary tubulointerstitial damage
Humoral mediated - antibodies
Cell mediated - T cells, inflamm cells, complement

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6
Q

Damage to endothelial or mesangial cells leads to:

A

Proliferative lesion

Haematuria

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7
Q

Damage to epithelial or podocytes leads to:

A

Non-proliferative lesion

Proteinuria

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8
Q

Diagnosis of GN

A 
Clinical
Bloods
Urinalysis
Urine microscopy - casts, RBCs
Urine protein:creatinine ratio
Biopsy
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9
Q

Microalbuminuria

A

30-300mg/day

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10
Q

Asymptomatic proteinuria

A

Less than 1g/day

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11
Q

Heavy proteinuria

A

1-3g/day

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12
Q

Nephrotic proteinuria

A

More than 3g/day

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13
Q

Dysmorphic RBCs

A

From UUT

Red cells escaping GBM = squished

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14
Q

Isomorphic RBCs

A

From LUT

Round

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15
Q

Red cell casts

A

Always pathological

Nephritic syndrome

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16
Q

Is nephrotic syndrome proliferative or non-proliferative?

A

Non-proliferative = proteinuria

Damage to podocytes/epithelium

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17
Q

Complications of nephrotic syndrome

A 
Infection
Renal vein thrombosis
PE
Volume depletion
Vit D deficiency
Sub-clinical hypothyroid
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18
Q

Is nephritic syndrome proliferative or non-proliferative?

A

Proliferative = haematuria

Damage to endothelium/mesangial cells

19
Q

Focal GN

A

less than 50% affected

20
Q

Diffuse GN

A

> 50% affected

21
Q

Global GN

A

All of glomerulus affected

22
Q

Segmental GN

A

Part of glomerulus affected

23
Q

Crescents

A

Extra-capillary proliferation of inflammatory cells in Bowman’s space, e.g. RPGN in vasculitis, due to break in GBM from ANCA = compression and ischaemia

24
Q

Non immunosuppressive treatment of GN

A 
Anti-HT (aim for 130/80 or 120-75 for proteinuria)
ACEI/ARB
Diuretic
Statin
Anticoag/aspirin
Omega 3/fish
25
Q

Immunosuppressive treatment of GN

A

Steroids
Azathioprine
Alkylating agents (cylcophosphamide/chlorambucil)
Calcineurin inhibitors (tacrolimus/cyclosporin)
Mycophenolate
Plasmapheresis
IV IG, MABs

26
Q

Treatment of nephrotic syndrome

A 
Fluid and salt restriction
Diuretic
ACEI/ARB
Anticoagulant
IV albumin (if low volume)
Steroids + another immsup agent
27
Q

Types of primary idiopathic GN

A 
Minimal change GN
FSGS
Membranous GN
Membranoproliferative GN
IgA nephropathy
RPGN
28
Q

Minimal change GN

A

Commonest cause of nephrotic syndrome in kids
Non-proliferative - podocyte side
Does NOT cause progressive renal failure
IL-13

29
Q

Biopsy of minimal change GN

A

Normal on LM and IF

Foot process fusion on EM

30
Q

Treatment of minimal change GN

A

Steroids

Cyclophosphamide/MAB

31
Q

FSGS

A

Commonest cause of nephrotic syndrome in adults
Primary (most common) or secondary to HIV/heroin/obesity/reflux
Non-proliferative - podocyte side
50% progress to ESRF after 10 years
suPAR

32
Q

Biopsy of FSGS

A

FSGS on LM
Ig/Complement deposition on IF
Podocyte effacement

33
Q

Treatment of FSGS

A

Steroids

LT calcineurin inhibitors

34
Q

Membranous GN

A

2nd commonest cause of nephrotic syndrome in adults
Primary or secondary to Hep B/carcinoma/lymphoma/SLE/CTD
30% progress to ESRF after 10 years
Anti-PLA2r Ab
Non-proliferative = podocytes

35
Q

Biopsy of Membranous GN

A

Immune complex deposition in basement membrane on LM

Thickened BM

36
Q

Treatment of Membranous GN

A

Steroids
Alkylating agents (cyclophosphamide)
MABs

37
Q

IgA nephropathy

A 
Commonest GN in the world
Broad spec (microhaematuria and
38
Q

What is IgA nephropathy associated with?

A

Colitis, arhtritis, HSP

39
Q

Biopsy of IgA nephropathy

A

Mesangial cell proliferation and expansion on LM
IgA deposits in meseangium on IF
Increased inflammatory cells

40
Q

Treatment of IgA nephropathy

A

BP control
ACEI/ARB
Fish oil

41
Q

RPGN

A

Treatable cause of AKI
Rapid deterioration over days/weeks
Urinary sediment (RBCs, casts) and crescents

42
Q

ANCA positive RPGN

A

Vasculitis
GPA
MPA

43
Q

ANCA negative RPGN

A

Goodpasture’s
HSP
SLE

44
Q

Treatment of RPGN

A

Prompt immunosuppression: steroids, aza/cyclophosphamide/mycophenolate, MAB
Plasmapheresis
Supportive dialysis

Renal (19 decks)

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