Nephrology Flashcards

1
Q

Investigations when assessing glomerulonephritis

A

Blood- FBC, U&Es, LFT, CRP, immunoglobulins, electrophoresis, complement- C3 and C4, autoantibodies- ANA, ANCA, anti-dsDNA, anti-GBM, blood culture, hepatitis serology, ASOT (for strep)
Urine- MC&S, Bence Jones proteins, RBC casts, A:CR, P:CR
Imaging- CXR, renal ultrasound
Renal biopsy- required for diagnosis

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2
Q

Nephritic causes of glomerulonephritis

A
IgA nephropathy
Henoch-Schonlein purpura 
Post- streptococcal 
Anti-GBM disease
Rapidly progressive GN
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3
Q

What is Berger’s disease?

A

IgA nephropathy

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4
Q

Clinical picture of IgA nephropathy

A
Mesangial deposition of IgA complexes 
Occurs around 12-72 hours after infection- usually URTI
Young men classically
Macroscopic haematuria 
Associated with HSP and coeliac
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5
Q

Features of Henoch-Schonlein purpura

A
Small vessel vasculitis 
Palpable pruritic rash
IgA nephropathy and deposition in skin, joints and gut 
Abdominal pain
Polyarthritis
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6
Q

Treatment of IgA nephropathy

A

Supportive- fluids and analgesia
ACE-i/ ARB to reduce the proteinuria and protect the renal function
Corticosteroids if persistent

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7
Q

Diagnosis of IgA nephropathy

A

Renal biopsy showing IgA deposition in the mesangium

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8
Q

Clinical features of post- streptococcal glomerulonephritis

A

1-2 weeks after streptococcal infection
Evidence of streptococcal infection- low C3 complement levels, raised ASOT and anti-DNAase B
Immune complex formation and inflammation in the glomerulus

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9
Q

Treatment for post-streptococcal GN

A

Supportive

Abx to clear the streptococcus

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10
Q

Auto-antibodies in anti-GBM disease

A

Type IV collagen

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11
Q

Presentation of anti-GBM disease

A

Renal disease- oliguria/ anuria, haematuria, AKI, renal failure
Lung disease- pulmonary haemorrhage, SOB, haemoptysis

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12
Q

Treatment for anti-GBM disease

A

Plasma exchange
Corticosteroids
Cyclophosphamide

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13
Q

Causes of rapidly progressive GN

A

Small vessel/ ANCA vasculitis
Lupus nephritis
Anti-GBM antibodies

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14
Q

Primary aetiology of nephrotic syndrome

A

Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN

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15
Q

Secondary aetiology of nephrotic syndrome

A
DM
Lupus nephritis 
Myeloma 
Amyloid
Pre-eclampsia
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16
Q

Proteinuria results from

A

Podocyte pathology

17
Q

Management of nephrotic syndrome

A

Reduce oedema- fluid and salt restriction, diuresis with loop diuretics
Renal biopsy and then treatment of underlying cause
Biopsy avoided in children unless no response to steroids (not minimal change disease in this case)
Reduce proteinuria- ACE-i/ARB
Heparin/ warfarin

18
Q

Treatment for minimal change disease

A

Prednisolone 1mg/kg

19
Q

Drugs associated with minimal change disease

A

Lithium

NSAIDs

20
Q

Commonest glomerulonephritis seen on renal biopsy

A

Focal segmental glomerulosclerosis FSGS

21
Q

Secondary causes of FSGS

A
HIV
Heroin
Lithium
Lymphoma
Any cause of decreased kidney mass or number of nephrons- other glomerulonephitides
22
Q

Treatment of FSGS

A

ACE-i/ARB and blood pressure control in all

Corticosteroids in primary disease

23
Q

Presentation of lupus nephritis

A
Rash
Photosensitivity
Ulcers
Arthritis
Serositis
CNS effects
Cytopenias 
Renal disease- nephropathy is common
24
Q

Triad in haemolytic uraemic syndrome

A

Haemolytic anaemia
Low platelets
AKI with haematuria/proteinuria

25
Q

Classical secondary cause of haemolytic uraemic syndrome

A

Shiga toxin producing Escherichia coli 0157:H7