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Nephrology > GLomerulonephritis > Flashcards

GLomerulonephritis Flashcards

1
Q

Where is the site of pathology in nephrotic vs nephritic syndrome?

A

Nephroitic syndrome is characterized by an inability to prevent protein from getting through the glom
- therefore problem is with the podocyte / podocyte foot processes

nephritic syndrome is due to problem with GBM

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2
Q

Nephrotic syndrome is associated with increased susceptibility to …?

A

Infection

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3
Q

What is the first think to determine in a GN question?

A

Is this nephrotic vs nephritic syndrome

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4
Q

What are the typical hallmarks of nephrotic syndrome?

What are the typical hallmarks of nephritic syndrome?

A

Proitinuria ACR >300

Haematuria + protinuria + HTN

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5
Q

Pt has normal appearing (not dysmorphic) red cell casts. What is the site of origin of these?

A

These are not glomerular casts, must be from distal in the urinary tract

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6
Q

What is the feature of red cell cast from glom (ie from nephritic syndrome)?

A

dysmorphic red cell casts

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7
Q

What is the typical urine sediment in nephrotic syndrome?

A

Basically lots of lipids/fat
- Lipid droplets
- oval fat bodies
- lipid laden casts
- cholesterol crystals

Will not seen fat / lipids in nephritic syndrome

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8
Q

What is the typical urine sediment in nephritic syndrome?

A

Dysmorphic red cell casts, White cell casts, white blood cells

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9
Q

Can a urine dipstrick detect microalbuminuria?
Can a urine dip detect high levels of immunoglobulins in the urine?

A

No, can only detect macroalb
No, can only detec alb not other protiens

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10
Q

What is primary GN vs secondary GN?

A

Primary is when the GN occurs in isolation (ie an idiopathic GN)
secondary is as a result of a systemic disease such as SLE

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11
Q

For exam purposes, what is the only disease (primary or secondary) that can present with both nephrotic and nephritic?

A

IgA nephropathy
Lupus nephritis
- Nephrotic = lupus class V (membranous)
- Nephritic = immune complex lupus nephritis calss III/IV

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12
Q

What are some common primary GN causing nephroitic syndrome?
What are some common secondary GN causing nephroitic syndrome?

A

Primary:
- Minimal change disease
- Membranous nephropathy
- FSGS

Secondary
- Diabetic nephropathy
- Amyloid, infection, drug, malignancy

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13
Q

What are some common primary/secondary GNs causing nephritic syndrome?

A
  • Anti GBM
  • Immune complex related: Infection related, IgA, Lupus, Cryoglobulinaemia
  • Immune complex: Lupus nephritis class III/IV
  • Monoclonal immunoglobulin associated GN (ie C3 GN)
  • TMA (TTP, HUS, aHUS, APS, Scleroderma)
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14
Q

Which nephrotic syndrome GN occurs in childhood? which occur in adulthood mostly?

A

Minimal change
Membranous, DM GN

FSGS occurs at all ages

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15
Q

woman in 30s, nephritic syndrome. What is the most likely cause?

A

Lupus nephritis or IgA

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16
Q

Which nephritic syndrome GN occurs mostly in young adults? which occur in adulthood mostly?

A

Lupus nephritis, IgA nephropathy

ANCA vasculitis occurs later in life

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17
Q

woman in 70s, nephritic syndrome. What is the most likely cause?

A

ANCA vasculitis

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18
Q

Layers of the glom from endo to epithelial?

A

endothelium
GBM
Podocytes

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19
Q

the GBM is selective for molecules base on what properties of the molecule?

A

Charge and size
- ie large very polar molecules dont pass through

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20
Q

What are the main findings in mesangial cell diseases? what are some common mesangial cell diseases?

A

Diseases of the mesangial cells cause haematuria
- ie if someone has just protein in the urine then the mesangial cells are unlikely to be significantly involved

Common diseases with a prediliction for mesangial cells:
- IgA nephropathy, IgM nephropathy
- Mesangioproliferative nephropathy
- Class II lupus nephritis
- Diabetic nephroipathy (can present in other ways too)

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21
Q

What are the main findings in diseases targeting the podyocytes / epithilial layer? what are some common examples?

A

Findings:
- nephrotic syndrome (ie isolated protinuria)

Diseases:
- Minimal change
- Membranous
- FSGS
- Class V lupus nephritis
- Diabetic nephropathy

22
Q

What are the main findings in diseases targeting the endothelial layer? what are some common examples?

A

Diseases that target the endothelial layer are usually aggressive and involve lots of immune activation because they are in contact with the blood
- these usually cauise nephritic syndrome (protein and blood in urine)

Examples:
- infection associated GN
- Mesangioproliferative GN
- Class III and IV lupus
- Anti GMB disease vasculitis and cryoglobulinaemia
- HUS

23
Q

Essential features of minimal change disease (inc Rx)?

A

Pure nephrotic syndrome
- Generalised oedema, low protein and lipids
- Urine ACR high, inactive sediment (lipid sediment)
Presents in childhood
Renal Bx:
- normal light micro (ie minimal change)
- EM showing flattened podocytes / effacement

Steroids (very responsive)

24
Q

Is minimal change worse in children or adults?

A

Adults

25
Q

Minimal change exists on a spektrum with…?

A

FSGS

26
Q

If minimal change is not responding to steroids, then need to consider which alternative Dx?

A

FSGS (more severe on same spektrum)
Usually not as steroid responsive

27
Q

What histo features for FSGS?

A

Focal glom involvment - only some of the gloms are affected
- Usually the juxtamedullary gloms first

Sentimental glom involvement - only part of the glom is involved

Change include glomerular sclerosis (its in the name), and hyalinosis
Can also have interstitial fibrosis (worse prog factor because already have irreversible damage)

28
Q

Pt has transplant, gets AKI and GN is suspected. What is the most common GN post transplant?

A

FSGS

29
Q

Is FSGS always primary?

A

No
Can occur primary or secondary

30
Q

Treatment of FSGS?

A
  • Steroids high dose
  • CNI - tac or cyclosporin if not responding
31
Q

Essential features of membranous nephropathy (inc Rx)?

A

Adult presentation
Nephrotic syndrome, blood pressures can be normal

Histology
- Light micro: Thickened GBM
- IF: granular IgG +/- C3
- AM subepithilial deposits (this is what makes GBM thickened)
- Silver spikes

Treatment is via risk stratification (there is a big spektrum of disease severity)
Risk stratify based on:
- degree of protinuria
- Degree of renal impairment
- Titre of PLA2R ab

Treatment:
- High/very high risk: cyclical methylpred and cyclophosphamide

32
Q

What is the one case of GN where serological testing often confirms the Dx? What is tested for?

A

Membranous
- PLA2R abs

Can also be used for monitoring response to Rx

33
Q

What complication are pts with membranous nephropathy particularly at risk of? (all nephrotic syndrome with low albumin are at risk of this?

A

VTE
- membranous is most at risk relative to other nephrotic syndromes

34
Q

WHo should be anticoagulated nephrotic syndrome? what agent is used?

A

Pts with Alb <20, who have a clot (ie renal vein thrombosis) or who are at very high risk of VTE

If low risk of bleeding then warfarin
If high risk of bleeding then aspirin

If albumin improved with treatment then this will reduce their thrombotic risk

They should all be on prophylactic clexane

35
Q

What is the range of IgA nephropathy presentations and what is a main prognostic factor that determines the severity of IgA nephropathy?

A

Presentation is variable
- Asymptomatic haematuira
- Synpharingitic haematuria
- Rapidly progressive GN (crecentic GN)

Degree of protinuria is the most important prognostic factor
- Ie high protiunuria with crecents on Bx is worst prognosis

35
Q

Pt has henoch Shonlein pupura and new renal impairment. What type of GN?

A

Secondary IgA nephropathy
- HSP is IgA vasculitis, these pts can get secondary IgA nephropathy

36
Q

What is the most common form of primary GN?

A

IgA Nephropathy

37
Q

Explain the pathyphys of IgA Nephropathy?

A

Plasma cell makes IgA that is abnormal (hyperglycosylated in the hinge region)

Bodies immune system recognizes that this IgA is not normal -> IgA attaches to the hing region forming and IgA/IgG immune complex

This complex has a prediliction for deposition in the kidney, resulting in IgA Nephropathy

38
Q

Should steroids be used to treat IgA nephropathy?

A

Unclear, in exam say no
- There is most likely to be a role in severe IgA Nephropathy however studies are ongoing

Pick ACEI/ARB (supportive care) as the answer

39
Q

Elderly pt. Unwell with AKI and systemic features (including skin features). Protein and blood in urine. What is Dx?

A

ANCA vasculitis (probably PR3 ANCA if very unwell / rapidly progressive)

40
Q

What are the classic RPGN/crecentic GNs?

A

ANCA GN
Anti GBM
Infection associated GN
Class IV/V lupus

41
Q

Pt has IgA staining postivie of GBM. What disease?
Pt has IgG staining positive of GBM. What disease?

A

IgA nephroipathy
Anti GBM (IgG mediated)

42
Q

GPA is most associated with which type of ANCA? What about EGPA?

A

PR3 (C-ANCA)
MPO (P-ANCA)

43
Q

Elderly pt with asthma has suspected GN. FOund to have eosinophils on bloods. What systemic condition and what is the marker?

A

EGPA - asthma, granulomas, eosiniphils

this is an ANCA vasculitis that can therefore cause GN
- EGPA associated with MPO ANCA (p-ANCA)

44
Q

Treatment of ANCA vasculitis?

A

Pulse methylpred followed by weaning pred
Rituxumab / cyclophosphamide

45
Q

What are teh types of lupus GN? Which ones are most severe and which ones would you treat?

A

Class 1 - normal / minimal disease
Class II - mesangial disease
CLass 3 - focal proliferative GN (nephritic)
Class 4 - Diffuse proliferative (nephritic)
Class 5 - membranous GN (Nephrotic)
Class 6

Class 3 and 4 are worst - always treated with immunosupression

Class 5 is bad when nephrotic range protinuria, but can exist with sub nephrotic range protinuria
- Treat with immunosupression if nephrotic range protinuria

46
Q

What is the treatment for lupus nephritis (ie clas II/IV +/- V)?

A

Pulse methylpred and CNI usually
- In women use mycophenylate because less fertility effects

47
Q

Main features of post infectious GN?

A
  • 2x subtypes: post infectious + GN associated with active infection
    -> post infectious: 1-6 weeks post strep infection. Post infectious is nephritic. Pts are usually well
    -> active infection: usually staph infections in older males with RF (DM, IVDU etc). Nephritic or RPGN, usually more unwell

Post infectious GN:
- Bloods showing low complement, ASOT + (antistreptolysin titre), anti DNAse B antibodies

EM showing humps and lumps

Treatment supportive, limited role for steroids

48
Q

What conditions typically causes membranoproliferative GN pattern?

A

Complement (C3) GN
Monoclonal Ig associated GN
Cryoglobulinaermic GN

49
Q

Next step if see MPGN pattern on Bx?

A

IF - looking for complement and immunoglobulins

Complement only (C3 or C4) = complement glomerulopathy

Positive Ig +/- C3
- Monoclonal gammopathies
- Autoimmune disease (lupus)

Negative for Complement and Ig
- APS
- HUS/TMA

Nephrology (3 decks)

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