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
Immunosuppressive treatment of GN
Steroids Azathioprine Alkylating agents (cylcophosphamide/chlorambucil) Calcineurin inhibitors (tacrolimus/cyclosporin) Mycophenolate Plasmapheresis IV IG, MABs
26
Treatment of nephrotic syndrome
``` Fluid and salt restriction Diuretic ACEI/ARB Anticoagulant IV albumin (if low volume) Steroids + another immsup agent ```
27
Types of primary idiopathic GN
``` Minimal change GN FSGS Membranous GN Membranoproliferative GN IgA nephropathy RPGN ```
28
Minimal change GN
Commonest cause of nephrotic syndrome in kids Non-proliferative - podocyte side Does NOT cause progressive renal failure IL-13
29
Biopsy of minimal change GN
Normal on LM and IF | Foot process fusion on EM
30
Treatment of minimal change GN
Steroids | Cyclophosphamide/MAB
31
FSGS
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
Biopsy of FSGS
FSGS on LM Ig/Complement deposition on IF Podocyte effacement
33
Treatment of FSGS
Steroids | LT calcineurin inhibitors
34
Membranous GN
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
Biopsy of Membranous GN
Immune complex deposition in basement membrane on LM | Thickened BM
36
Treatment of Membranous GN
Steroids Alkylating agents (cyclophosphamide) MABs
37
IgA nephropathy
``` Commonest GN in the world Broad spec (microhaematuria and ```
38
What is IgA nephropathy associated with?
Colitis, arhtritis, HSP
39
Biopsy of IgA nephropathy
Mesangial cell proliferation and expansion on LM IgA deposits in meseangium on IF Increased inflammatory cells
40
Treatment of IgA nephropathy
BP control ACEI/ARB Fish oil
41
RPGN
Treatable cause of AKI Rapid deterioration over days/weeks Urinary sediment (RBCs, casts) and crescents
42
ANCA positive RPGN
Vasculitis GPA MPA
43
ANCA negative RPGN
Goodpasture's HSP SLE
44
Treatment of RPGN
Prompt immunosuppression: steroids, aza/cyclophosphamide/mycophenolate, MAB Plasmapheresis Supportive dialysis