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Renal > Glomerulonephritides > Flashcards

Glomerulonephritides Flashcards

1
Q

Types of glomerulonephritis

A

Spectrum from nephrosis (proteinuria due to podocyte pathology) to nephritis (haematuria due to inflammatory damage)
Can be confusing picture as nephritis can lead to nephrosis

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2
Q

Renal biopsy preparation

A

BP <160/95
Hb >9, plt>100
Stop anticoagulants (aspirin 1wk, warfarin to PT<1.2, LMWH 24h)

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3
Q

Renal biopsy post-procedure care

A

Bed rest 4h minimum
Monitor pulse, BP, symptoms, urine colour
Don’t discharge until visible haematuria settled

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4
Q

Renal biopsy interpretation

A

Proportion of glomeruli involved (focal/diffuse)
How much of individual glomeruli affected (segmental/ global)
Hypercellularity
Sclerosis
Immunohistology for deposits (Ig, light chain, complement)
EM for podocytes, deposit locations

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5
Q

IgA nephropathy presentation

A

Asymptomatic non-visible haematuria 12-72h post infection

Slow disease, renal failure in 50% after 30yrs

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6
Q

IgA nephropathy diagnosis

A

Renal biopsy shows IgA deposition in mesangium

Proteinuria <1g

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7
Q

IgA nephropathy treatment

A

RAS blockers reduce proteinuria + protect renal function

Corticosteroids + fish oil if persistent proteinuria >1g after 3-6mths RAS blocker and GFR >50

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8
Q

What is HSP

A

Henoch-Schonlein purpura, small vessel vasculitis with IgA deposition in skin/ joints/ gut in addition to kidney

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9
Q

HSP presentation

A

Purpuric rash on extensor surfaces (typically legs)
Intermittent polyarthritis
Abdo pain
Nephritis

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10
Q

HSP diagnosis

A

Clinical usually
Confirmed with +ve IF for IgA and C3 in skin
Renal biopsy identical to IgA nephropathy

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11
Q

HSP treatment

A

Same as IgA nephropathy for renal disease

Steroids may be used for gut involvement

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12
Q

What is Post strep GN

A

2wks post throat/ 4-6wks post skin infection, strep antigen deposits in glomerulus causing immune complex formation

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13
Q

Post strep GN presentation

A 
Haematuria
Acute nephritis (oedema, inc BP, oliguria)
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14
Q

Post strep GN diagnosis

A

Evidence of strep infection

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15
Q

Post strep GN treatment

A

Supportive

Abx to clear nephritogenic bacteria

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16
Q

What is Anti-GBM disease

A

Previously known as Goodpasture’s, auto-Abs to type IV collagen which makes up glomerular and alveolar basement membranes

17
Q

Anti-GBM disease presentation

A

Oliguria, haematuria, AKI

Pulmonary haemorrhage -> SOB, haemoptysis

18
Q

Anti-GBM disease prognosis markers

A

Dialysis-dependence at presentation

Increased crescents on renal biopsy indicate poorer prognosis

19
Q

Anti-GBM disease diagnosis

A

Anti-GBM in circulation/kidney

20
Q

Anti-GBM disease treatment

A

Plasma exchange
Corticosteroids
Cyclophosphamide

21
Q

Rapidly progressive GN causes

A

Small vessel/ANCA vasculitis
Lupus nephritis
Anti-GBM disease
IgA/membranous nephropathy may transform to become rapidly progressive

22
Q

Rapidly progressive GN diagnosis

A

GBM breaks allowing inflammatory cell influx

Crescents seen on renal biopsy

23
Q

Rapidly progressive GN treatment

A

Corticosteroids
Cyclophosphamide
Treat cause

24
Q

Nephrotic syndrome definition

A

Proteinuria >3g/24h (P:CR >300, A:CR >250)
Hypoalbuminaemia <30g/L
Oedema

25
Q

Nephrotic syndrome causes

A

1˚ renal disease: minimal change disease, membranous nephropathy, FSGS
2˚ causes: DM, SLE, myeloma, amyloid, pre-eclampsia

26
Q

Nephrotic syndrome presentation

A

Generalised pitting oedema

Systemic symptoms from causes of 2˚

27
Q

Nephrotic syndrome management

A 
Reduce oedema (<1L fluid/d + salt restriction + diuretics if needed)
Treat underlying cause (renal biopsy, steroids first in children as minimal change is most likely)
Reduce proteinuria (anti-RAS)
Manage complications (VTE, infection, hyperlipidaemia)
28
Q

Minimal change disease presentation

A

Idiopathic or associated with NSAIDs/lithium or paraneoplastic
Doesn’t cause renal failure

29
Q

Minimal change disease diagnosis

A

EM shows thinning of podocyte foot processes

30
Q

Minimal change disease treatment

A

Prednisolone 1mg/kg for 4-16 wks

Frequent relapses managed with inc dose or cyclophosphamide/ calcineurin inhibitors

31
Q

What is FSGS

A

Commonest GN seen on renal biopsy

Can be 1˚ or 2˚ (HIV, heroin, lithium, lymphoma)

32
Q

FSGS diagnosis

A

Glomeruli have focal sclerosis on biopsy

If <10 glomeruli in biopsy sample then early disease may be missed

33
Q

FSGS treatment

A

anti-RAS and BP control
Corticosteroids in 1˚ disease
Calcineurin inhibitors 2nd line
Plasma exchange + rituximab used for recurrence in transplants

34
Q

Membranous nephropathy causes

A

Idiopathic 1˚

2˚ to:
malignancy (lung, GI, breast, prostate, haem)
infection (hep B/C, strep, malaria, schistosomiasis)
auto-immune (SLE, RA, sarcoidosis, Sjogren’s)
drugs (gold, penicillamine)

35
Q

Membranous nephropathy diagnosis

A

Diffusely thickened GBM due to subepithelial deposits
Anti-phospholipase A2 receptor in 75% of 1˚ disease
Spikes on silver stain

36
Q

Membranous nephropathy treatment

A

anti-RAS and BP control
Corticosteroids + cyclophosphamide/chlorambucil for those at high risk of progression (proteinuria >4g with no response to anti-RAS over 6 mths or 30% creatinine increase with GFR > 30)
Treat underlying cause for 2˚ disease

37
Q

Membranoproliferative glomerulonephritis types

A

Immune-complex associated - abnormal immune complexes deposit in kidney + activate kidney, often underlying cause e.g. infection/ autoimmune

C3 glomerulopathy - Genetic/acquired defect in alternative complement pathway e.g. C3 nephritic factor, progressive kidney dysfunction common

38
Q

Membranoproliferative glomerulonephritis diagnosis

A

Proliferative glomerulonephritis with electron dense deposits
Ig deposition distinguishes between types

39
Q

Membranoproliferative glomerulonephritis treatment

A

anti-RAS and BP control

Underlying cause in immune-complex disease, immunosuppression trial if none found

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