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Flashcards in Glomerulonephritis Deck (54)
1

What is GN?

Immune mediated disease of the kidneys affecting the glomeruli (with secondary tubulointerstitial damage)

2

Damage to endothelial or mesangial cells leads to which type of lesion?

Proliferative lesion and red cells in urine

3

Damage to podocytes leads to which kind of lesion?

Damage to podocytes leads to a non-proliferative lesion and protein in the urine

4

Urinalysis findings of glomerulonephritis?

Haematuria, proteinuria

5

Urine microscopy would show what in glomerulonephritis?

RBC (dysmorphic), RBC and granular casts, lipiduria

6

Haematuria in GN presentation

Episodes of painless macroscopic haematuria

7

Nephrotic syndrome

>3g protein per day

8

Heavy proteinuria

1-3g/day

9

Asymptomatic proteinuria

<1g per day

10

Microalbuminuria

30-300mg albuminuria/day

11

Red cell casts are pathogonomic of what?

GN

12

Red blood cells in GN?

Dysmorphic

13

Acute Renal Failure
Oliguria
Oedema/ Fluid retention
Hypertension
Active urinary sediment
RBC’s, RBC & Granular Casts

Indicative of a proliferative process

Nephritic syndrome

14

Proteinuria  3 g/day (mostly albumin, also globulins)
Hypoalbuminaemia (<30)
Oedema
Hypercholesterolaemia
Usually normal renal function

Indicative of a non proliferative process

Nephrotic syndrome

15

Hypercholesterolaemia in nephritic or nephrotic syndrome?

Nephrotic

16

Nephrotic syndrome complications?

Infections - loss of opsonising antibodies
Renal vein thrombosis
Pulmonary emboli
Volume depletion (overaggressive use of diuretics) - may lead to ARF (pre-renal)

Vit D deficiency
Subclinical hypothyroidism

17

Most common cause of glomerulonephritis?

Idiopathic

18

Systemic diseases associated with glomerulonephritis?

ANCA associated systemic vasculitis
Lupus
Goodpastures
HSP

19

Proliferative or non-proliferative

usually refers to presence or absence of proliferation of mesangial cells

20

Focal/diffuse

< or > 50% of glomeruli affected

21

Global/segmental

All or part of glomerulus affected

22

Crescenteric

Presence of crescents - epithelial cell extracapillay proliferation e.g. RPGN in vasculitis

(RPGN = rapidly progressing glomerulonephritis)

23

Easier explanation of crescenteric glomerulonephritis?

Crescenteric more often seen in conditions like Goodpastures and systemic vasculitis
(crescenteric GN = when there is an accumulation of cells outside the capillary loops, but within the Bowman’s capsule)
-Presents as RPGN

24

Treatment of GN
(non-immunosuppression)
DASH

DASH
Diuretics
ACEi/ARB
Steroids
anti-Hypertensives

25

Treatment of GN (immunosuppression)

Drugs
Corticosteroids (Prednisolone po/MethylPred IV)
Azathioprine
Alkylating agents (Cyclophosphamide/ Chlorambucil)
Calcineurin inhibitors (Cyclosporin/Tacrolimus)
Mycophenolate Mofetil (MMF)


Plasmaphoresis: TPE (therapeutic plasma exchange)

Antibodies: IV immunoglobulin
Monoclonal T or B cell antibodies

26

General treatment of nephrotic patients

Fluid restriction
Salt restriction
Diuretics
ACE inhibitors/ARBs

?anticoagulation
IV albumin (only if volume deplete)

27

What is complete remission?

Proteinuria <300mg/day

28

What is partial remission?

Proteinuria <3g/day

29

What is partial remission?

Proteinuria <3g/day

30

Commonest cause of nephrotic syndrome in children

Minimal change nephropathy

31

Biopsy, ML & IF and EM findings of minimal change nephropathy

Normal biopsy
Normal LM & IF
Foot process fusion on EM

32

How to treat minimal change nephropathy

94% remission with oral steroids

Second-line drugs: cyclophosphamide/CSA

(some are steroid resistant/dependent or have multiple relapses

33

Does not cause progressive renal failure
Possibly caused by IL-13

Minimal change nephropathy

34

Commonest cause of nephrotic syndrome in adults (35%)
10 or 20 (HIV/Heroin use/Obesity/ Reflux nephropathy)
Renal biopsy: As its name describes on light microscopy with minimal Ig/ Complement deposition on IF
Remission with prolonged steroids in 60 %
50 % progress to end stage renal failure after 10 years

Focal Segmental Glomerulosclerosis

35

Risk factors for FSGS

HIV/heroin use/obesity/reflux nephropathy

36

Renal biopsy findings of FSGS

Focal segmental glomerulosclerosis (as the name tells you lol)

Minimal Ig/complement deposition on IF

37

Treatment of FSGS

Remission with prolonged steroids in 60%

50% progress to end stage renal failure after ten years

38

New data implicating soluble urokinase plasminogen activator receptor (suPAR).
Upregulate integrins (cell signalling molecules).
Podocyte effacement.
67% of patients have increased suPAR levels.

FSGS

39

2nd commonest cause of nephrotic syndrome in adults (15-30%)
10 or 20
Important 20 causes include:
infections (hepatitis B/ parasites)
connective tissue diseases (lupus)
malignancies (carcinomas/ lymphoma)
drugs (gold/penicillamine)
Renal biopsy: subepithelial immune complex deposition in the basement membrane
Steroids/ Alkylating agents/B cell monoclonal Ab
30% progress to end stage renal failure in 10 years

Membranous nephropathy

40

Causes of nephropathy

Infections (hep B/parasites)

Connective tissue diseases (lupus)

Malignancies (carcinomas/lymphoma)

Drugs (gold/penicillamine)

41

Renal biopsy findings in membranous nephropathy

Subepithelial immune complex deposition in the basement membrane

42

Treatment for membranous nephropathy?

Steroids
Alkylating agents
B cell monoclonal antibodies

-30% progress to end stage renal failure in 10 years

43

Anti PLA2r antibody

Present in >70% cases of primary membranous nephropathy

44

Thickened basement membrane on silver stain?

Membranous nephropathy

45

What does the basement membrane look like in membranous nephropathy? and what stain would you use?

Thickened basement basement membrane using silver stain

46

Commonest GN in the world?

IgA nephropathy

47

Associated with HSP

IgA nephropathy
(remember HSP is IgA complex mediated anyway)

48

Renal biopsy findings of IgA nephropathy?

Mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on IF

49

Drugs used in IgA nephropathy?

BP control
ACEi & ARB
Fish oil

50

Which stain would show mesangial cell proliferation and expansion?

H&E stain

51

A treatable cause of acute renal failure
Rapid deterioration in renal function over days/weeks
Active urinary sediment (RBC’s, RBC & Granular Casts)
May be part of systemic disease.
Associated with glomerular crescents on biopsy.

Rapidly progressing glomerulonephritis
(RPGN)

52

How do you detect ANCA? (anti-neutrophil cytoplasmic antibodies)

Immunofluorecence

53

Treatment for RPGN

Treatment must be prompt!
Strong immunosuppression with supportive care including dialysis if needed

54

Treatment for RPGN

Immunosuppression
Steroids (IV Methylprednisolone / Oral Prednisolone)
Cytotoxics (Cyclophosphamide/ Mycophenolate/ Azathioprine

Plasmapheresis