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BPT Flashcards > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

Clinical features of IgA nephropathy

A

Usually young male
Recurrent episodes of macroscopic haematuria
Typically associated with mucosal infections
Rarely has nephrotic range proteinuria

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2
Q

Diagnostic features of IgA nephropathy

A

Mesangial hypercellularity in histology
Positive immunofluorescence for IgA and C3

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3
Q

Clinical features of post-strep glomerulonephritis

A

URTI precedes GN - typically an interval of 1-6 weeks
Nephritis syndrome
- haematuria (tea, cola-coloured urine)
- hypertension
- oedema
Associated with LOW C3 and normal C4 levels levels

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4
Q

GN that can recur

A

IgA nephropathy (most common)
FSGC (most rapid)
Membranoproliferative GN (Mesangiocapillary)
Membranous GN

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5
Q

Features of lupus nephritis

A

Proteinuria
Haematuria
Hypertension
Oedema
Reduced kidney function
Renal colic or flank pain
Fever and fatigue

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6
Q

What GN is associated with low C3 levels

A

Poststreptococcal GN
Lupus nephritis
Membranoproliferative GN

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7
Q

Histological features of proliferative lupus nephritis

A

Subendothelial immune deposits/wire loops
Hypercellularity
Leukocyte infiltration
Fibrinoid necrosis
Hyaline thrombi
Crescents in severe LN

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8
Q

Treatment of lupus nephritis

A

Immunosuppressants - steroids, cyclophosphamide, MMF, azathioprine
Biologics - rituximab, belimumab
ACE inhibitors
NSAIDs
Anticoagulants
Dietary and lifestyle changes
Dialysis or kidney transplant

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9
Q

Principle of treatment in lupus nephritis

A

Induction - prednisone, cyclophosphamide, MMF, rituximab (refractory cases)
Maintenance - MMF or azathioprine for at least 2 years post remission

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10
Q

Feature of pauci-immune rapidly progressive GN

A

Severe form of kidney disease
Characterised by inflammation of glomeruli and rapidly declining kidney function
Associated with autoimmune disorders

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11
Q

Treatment of pauci-immune RPGN

A

Immunosuppressive therapy - steroids, cyclophosphamide, rituximab
Plasmapheresis
Maintenance therapy
Supportive Care
Kidney transplant

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12
Q

Features of membranoproliferative GN

A

Nephrotic syndrome
Significant proteinuria
Haematuria with dysmorphic red cells and red cell casts**

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13
Q

Histology features of FSGS

A

Podocyte detachment leading to segmental sclerosis ***
Collapsing lesions
Hyalinosis
Adhesions

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14
Q

Clinical features of FSGS

A

Characterised by sclerosis affecting only some segments of glomeruli
Nephrotic syndrome

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15
Q

Poor prognostic markers of IgAN

A

Elevated serum Cr
HTN
Proteinuria > 1g/day

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16
Q

Clinical features of MN

A

Proteinuria (nephrotic range or sub-nephrotic range)
Microscopic haematuria
Normal or impaired renal function
HTN
Nephrotic syndrome **
Hyperlipidaemia *
Thromboembolic complications*

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17
Q

Secondary causes for MN

A

Lupus nephritis
Hepatitis B and C
Malignancy (lung, colon, stomach and kidney)
Medications (NSAIDs, gold, penicillamine)

18
Q

Biopsy results for MN

A

LM - immune complex deposition in basement membrane “spike and hold”
Granular staining for IgG

EM - electron dense deposits in GBM in subepithelial regions

19
Q

Antibodies present in MN

A

Anti-PLA2R (70-80% of primary cases), correlates with activity
THSD7a antibodies (in 3-5% of pts who were anti-PLA2R negative)

20
Q

GN most likely to rapidly recur

A

FSGS
Characterised by massive proteinuria within hours to days after implantation of new kidney

21
Q

Features of Alport’s syndrome

A

Progressive renal failure, hearing loss ** and ocular abnormalities **
Associated with corneal opacities, anterior lenticonus **

22
Q

Genetic mutation of Alport’s

A

COL4A5 (X-linked) or COL4A3 and COL4A4 (AR)
Results in absence of collagen IV a3a4a5 network

23
Q

Clinical features of TBMN

A

Persistent microhaematuria (most common cause of persistent haematuria)
NO proteinuria **
Normal renal function and BP
AD inheritance of haematuria **

24
Q

Histopathology features of TBMN

A

Uniform thinning of GBM

25
Q

Genetic mutation in TBMN

A

HETEROzygous COL4A3 or COL4A4 mutations

26
Q

Histological features of type 1 MGPN

A

Global and diffuse thickening of capillary walls
Caused by mesangial interposition into subendothelial zone of capillary loops - “train track formation”

27
Q

Types of MGPN

A

Type 1 - immune mediated
Type 2 - complement mediated, dense deposit disease

28
Q

Indications for renal biopsy in patients with suspected diabetic nephropathy

A

Rapid onset of proteinuria
Absence of retinopathy
Presence of haematuria
Active urinary sedment
Rapid decrease of renal function
Suspicion of other nephropathies secondary to systemic disease

29
Q

Clinical features of Goodpasture’s syndrome/anti-GBM

A

Pulmonary haemorrhage and rapidly progressive GN with renal failure

30
Q

Histopathology features of anti-GBM

A

Crescent formation, uniform age
IM - strong linear ribbon-like appearance of IgG

31
Q

Possible pathogenesis of hypercoagulable state in nephrotic syndrome

A

Decreased levels of antithrombin and plasminogen (due to urinary losses), increased platelet activation, hyperfibrinogenaemia, inhibition of plasminogen activation and presence of high molecular weight fibrinogen in circulation

32
Q

Causes of nephrotic syndrome

A

Idiopathic membranous nephropathy
Membranoproliferative GN
Minimal change disease

33
Q

Most common causes of secondary MCD

A

Medications (NSAIDs, selective COX-2 inhibitors)
Malignancy
Infection
Allergy

34
Q

Features of collapsing glomerulopathy

A

Segmental and global collapse of glomerular capillaries
Marked hypertrophy
Hyperplasia of podocytes

Most commonly seen in association with HIV
Also associated with TB, CMV, hepatitis B and hepatitis C

35
Q

Features of Chinese herbal nephropathy

A

Mild low-molecular-weight proteinuria
Hypertension
Severe anaemia
Development of uroepithelial atypia

36
Q

Histopathological features of CHN

A

Unusual extensive, virtually hypocellular cortical interstitial fibrosis
Associated with tubular atrophy and global sclerosis of glomeruli

37
Q

Histopathology findings on MCD

A

Minimal changes
Effacement of podocyte foot processes

38
Q

Management of MCD

A

Prednisone - very responsive

39
Q

Histology features of diabetic nephropathy

A

Thickening of GBM
Eosinophilic nodular glomerulosclerosis (Kimmelsteil-Wilson nodules)
Mesangial matrix expansion

40
Q

Histopathology scoring system for IgA nephropathy

A

MEST
Mesangial hypercellularity
Endocapillary hypercellularity
Segmental glomerulosclerosis
Tubullar atrophy/interstitial fibrosis

41
Q

Causes of FSGS

A

Can be idiopathic
Heroin
HIV infection
Sickle cell disease
Obesity
Interferon treatment
Congenital malformations i.e. CMT
NPHS1 and NPHS2 mutations

BPT Flashcards (32 decks)

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