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Y3M - Renal > Nephritic Syndrome > Flashcards

Nephritic Syndrome Flashcards

1
Q

Clinical presentation of nephritic syndrome.

A

AKI (GFR drops)

Haematuria (sometimes visible)

Mild to moderate oedema

Proteinuria < 3.5g

Hypertension

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2
Q

Give examples of nephritic syndromes.

A

Post-streptococcal GN

IgA nephropathy

Small vessel vasculitis (ANCA)

Anti-GBM

Thin Basement Membrane

Alport Syndrome

Lupus Nephritis

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3
Q

Investigation of nephritic syndrome.

A

Assess damage and potential cause

Bloods - FBC, U&Es, LFT, CRP, Immunoglobulins, Electrophoresis, COmplement, Autoantibodies, blood cultures, ASOT, Hepatitis serology

Urine - MC&S, Bence Jones proteins, RBC casts

Imaging - CXR and renal ultrasound

Renal biopsy

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4
Q

What is post-streptococcal GN caused by?

A

It occurs 1-2 weeks after a tonsillitis/pharyngitis infection or 3-4 weeks after impetigo/cellulitis.

It is a group A beta-haemolytic streptococcal infection.

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5
Q

Epidemiology of PS G.

A

Usually affects children ages 3-12 years

Can lead to RPGN

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6
Q

Presentation of PS GN.

A

Haematuria to acute nephritis with haematuria, oedema, hypertension and oliguria.

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7
Q

Investigations of PS GN.

A

Bloods

Biopsy

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8
Q

Investigation findings in PS GN.

A

+ve anti-streptococcal antibodies (ASO titre)

Low serum C3

anti-DNAse

Evidence of streptococcal infection

Immune complex deposition - IgG, IgM and C3 in the mesangium.

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9
Q

Treatment of PS GN.

A

Usually self-limiting

Treat infection

ACEi/ARB to treat hypertension and proteinuria.

Low sodium diet.

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10
Q

What is the most common GN worldwide?

A

IgA Nephropathy

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11
Q

Presentation of IgA nephropathy.

A

Episodic gross haematuria during or directly after URTI or GI infection, or strenous exercise.

Increased BP

Slow and indolent disease that causes renal failure within 30 years of diagnosis in 25-50% of cases.

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12
Q

Epidemiology of IgA Nephropathy.

A

Males > Females

2nd to 3rd decade of life usually

In workbook it says 25-30% of patients progress to ESRF within 20-25 years.

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13
Q

Worse prognosis in IgA Nephropathy.

A

Male

High BP

High crea

Proteinuria

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14
Q

Investigation findings in IgA nephropathy.

A

Asymptomatic microhaematuria with intermittent visible haematuria.

Increased serum IgA

Normal C3 and C4

On biopsy - IgA depositions in the mesangium

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15
Q

Treatment of IgA nephropathy.

A

Supportive therapy

ACEi/ARBs for proteinuria and hypertension

Corticosteroids might be considered if persistent proteinuria > 1g

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16
Q

Give examples of small vessel vasculites (ANCA +ve)

A

Granulomatosis with polyangiitis (Wegener’s)

Microscopic polyangiitis

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

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17
Q

Features of Granulomatosis with polyangiitis.

A

Renal disease leading to rapidly progressive GN with crescent formation, haematuria or proteinuria.

Pulmonary involvment with possible cough, haemoptysis or pleuritis.

Nasal obstruction

Ulcers

Epistaxis

Destruction of nasal septum -> Saddle-nose

Sinusitis

Skin purpura, nodules, peripheral neuropathy, mononeuritis multiplex, arthritis, eyes etc…

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18
Q

Investigation findings in Granulomatosis with polyangiitis.

A

cANCA (PR3) positive

Urinalysis with possible haematuria and proteinuria.

Biopsy - segmetal necrotising GN

CXR may show nodules and fluffy infiltrates of pulmonary haemorrhage

CT may show diffuse alveolar haemorrhage

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19
Q

Treatment of Granulomatosis with polyangiitis.

A

Severe disease - corticosteroids and cyclophosphamide or rituximab (this is to induce remission)

As maintenance methotrexate or azathioprine can be used.

Plasma exchange might be needed.

Co-trimoxazole as prophylaxis vs Pneumocystis jirovecii or Staphylococcal.

20
Q

What is microscopic polyangiitis?

A

Necrotising vasculitis affecting small and medium sized vessels.

21
Q

Symptoms of microscopic polyangiitis.

A

Rapidly progressive GN with pulmonary haemorrhage in 30%

Usually only mild resp symptoms.

22
Q

Investigation findings of microscopic polyangiitis.

A

pANCA (MPO) positive

Segmental necrotising GN

23
Q

Treatment of microscopic polyangiitis.

A

Steroids and methotrexate.

For maintenance use methotrexate, rituximab or azathioprine.

24
Q

What is Churg-Strauss syndrome?

A

A triad of adult-onset asthma, eosinophilia and vasculitis (+/- vasospasm, MI and DVT)

It affects the lungs, nerves, heart and skin.

You might see allergic rhinitis, purpura and peripheral neuropathy as well.

25
Q

Investigation findings in Churg-Strauss syndrome.

A

pANCA positive

Eosinophilia

Focal segmental necrotising GN

26
Q

Treatment of Churg-Strauss syndrome

A

Steroids

Rituximab if refractory disease

27
Q

What is anti-GBM disease?

A

Auto-antibodies to type IV collagen which is present in glomerular and alveolar basement membranes.

The antibody binds to the basement membrane and activates complement and proteases leading to disruption of filtration.

28
Q

Epidemiology of anti-GBM.

A

Two peaks.

3rd decade of life -> male > female

60+ -> female > male

29
Q

Pulmonary features of anti-GBM.

A

Reacts with pulmonary basement membrane as well causing pulmonary haemorrhage and haemoptysis.

30
Q

Presentation of anti-GBM.

A

Oliguria/anuria, haematuria, AKI, renal failure

Pulmonary haemorrhage, dyspnoea, haemoptysis

31
Q

Investigation findings of anti-GBM.

A

Anti GBM antibodies

Pulmonary infilrates on CXR

Biopsy showing linear deposition of IgG along basement membrane.

32
Q

Treatment of anti-GBM.

A

Plasma exchange to remove circulating anti-GBM antibodies

Corticosteroids to suppress inflammation

Cyclophosphamide to suppress further antibody synthesis.

33
Q

What is thin basement membrane disease?

A

Hereditary autosomal dominant disease.

Abnormalities of Type IV collagen

Good prognosis

34
Q

Ix findings of thin basement membrane disease.

A

Persistent microscopic haematuria

Possible intermittent visible haematuria

Diffuse thinning of GBM on biopsy.

35
Q

Treatment of thin basement membrane disease.

A

No known

Monitor renal function and supportive treatment.

36
Q

What is Alport syndrome?

A

X-linked mutation of COL4A5 gene which is supposed to code for type IV collagen.

37
Q

Features of Alport Syndrome

A

Haematuria

Proteinuria

Progressive renal insufficiency

Sensorineural hearing loss

Anterior lenticonus (bulging of lens on slit-lamp examination)

Macular and perimacular flecks

38
Q

Investigation findings of Alport Syndrome.

A

Persistent microscopic haematuria with intermittent visible haematuria

Sensorineural hearing loss

Splitting of GB and alternating thickening and thinning of GBM on biopsy.

FH

39
Q

Treatment of Alport Syndrome.

A

Supportive treatment

Renal replacement therapy

Renal transplant

40
Q

Complications of renal transplant in Alport Syndrome.

A

It can cause anti-GBM disease as the graft type IV Collagen is recognised as foreign.

41
Q

What is lupus nephritis?

A

Complication of SLE that can be both nephritic or nephrotic.

SLE is a systemic autoimmune disease with antibodies against nuclear components such as dsDNA.

There is deposition of antibody complexes causing inflammation and tissue damage.

42
Q

Presentation of lupus nephritis.

A

Rash

Photosensitivity

Ulcers

Arthritis

Serositis

CNS effects

Cytopenia

Renal disease

43
Q

Investigation findings in lupus nephritis.

A

ANA and anti-dsDNA positive

Biopsy can show 6 different classes of lupus nephritis with different presentations and slightly varying tx options.

44
Q

Treatment of lupus nephritis.

A

Class I and II -> mild changes and low risk of renal disease. ACEi/ARBs for renal protection and hydroxychloroquine for extra-renal disease.

Class III-V require immunosuppression. Mycophenolate, glucocorticoids, cyclophosphamide, rituximab.

45
Q

Supportive therapy of GN.

A

ACEi/ARBs for proteinuria

COntrol BP

Salt and water restriction if fluid overloaded

Diuretics

Consider LMWH if hypoalbuminaemic due to high risk of VTE

Statins for hypercholesterolaemia

46
Q
A

Y3M - Renal (11 decks)

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