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Year 2 > Kidney & systemic disease > Flashcards

Kidney & systemic disease Flashcards

1
Q

List the main multi-system diseases which involve the kidney

A 
Diabetes 
Vasculitis'
Renovascular disease
Myeloma
Lupus
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2
Q

Which type of diabetes can lead to diabetic nephropathy?

A

Type 1 AND type 2

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3
Q

How can we diagnose overt diabetic nephropathy?

A

Persistent albuminuria >300mg on two separate occasions at least 3-6months apart

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4
Q

Explain the pathogenesis of diabetic nephropathy

A

Glucose causes the release of vasoactive mediators which dilate the afferent arterioles of the kidney –>
Increased blood flow and thus GFR –>
Glucose stimulates growth factors causing kidney hypertrophy –>
Mesangeal expansion –>
Nodule formation (diabetic glomerulosclerosis) –>
Inflammation –>
Proteinuria (podocyte dysfunction) –>
Tubulo interstitial fibrosis

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5
Q

What do we call the nodules found within the kidney because of diabetes?

A

Kimmelstiel Wilson lesions

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6
Q

How long does diabetic nephropathy take to develop?

A

Roughly 15-20 years

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7
Q

How is diabetic nephropathy diagnosed?

A

Proteinuria
Other diabetic complications
Renal impairment

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8
Q

How is diabetic nephropathy managed?

A

Glycaemic control (HbA1c

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9
Q

How do ACE/ARBs help in diabetic nephropathy?

A

Dilate efferent arterioles in the kidney

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10
Q

What renal replacement therapies are available to diabetic patients?

A

Dialysis

Kidney +/- pancreas transplant

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11
Q

Who cannot get a combined kidney and pancreas transplant?

A

Type 2 diabetics

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12
Q

Define renovascular hypertension

A

Secondary hypertension usually caused by renal artery stenosis

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13
Q

What are the two main causes of renovascular disease? Which age groups get each?

A 
Fibromuscular dysplasia (young)
Artherosclerotic (old)
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14
Q

How does renal artery stenosis cause renovascular hypertension?

A

Hormonal and neuronal mechanisms increase blood pressure in response to reduced renal perfusion

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15
Q

Define ischaemic nephropathy

A

Reduced GFR associated with reduced renal blood flow beyond homeostatic correction

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16
Q

How does ischaemic nephropathy progress?

A

Renal atrophy then CKD

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17
Q

Which patients tend to get fibromuscular dysplasia?

A

Young women 15-50 y/o

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18
Q

In which case might you expect fibromuscular dysplasia to affect both renal arteries?

A

Familial fibromuscular dysplasia

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19
Q

List two conditions associated with fibromuscular dysplasia

A

Marfan’s syndrome

Ehlers Dantos

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20
Q

Which other important arteries, apart from the renal, can be affected in fibromuscular dysplasia?

A

Carotid (i.e carotid artery dissection)

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21
Q

Which patients tend to get artherosclerotic renal disease?

A

Old white men with CVS risk factors

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22
Q

How does renovascular disease present clinically?

A 
Hypertension
AKI after hypertension treatment (ACE/ARB)
CKD in elderly with vascular disease
Sudden onset pulmonary oedema
Microscopic haematuria 
Background arterial disease
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23
Q

What examination finding may be present in a patient with renovascular disease?

A

Abdominal bruit

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24
Q

How can ischaemic nephropathy be diagnosed?

A

USS
Artery duplex scans
CT/MR angiography
Angiogram

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25
Q

What is the characteristic radiological sign of fibromuscular dysplasia?

A

Corkscrewing of the arteries

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26
Q

How is renovascular disease managed?

A

BP control

Angioplasty +/- stenting

27
Q

Which blood pressure drugs should not be given in renal artery stenosis? Which other condition should these drugs not be given in?

A

ACE/ARB

Fibromuscular dysplasia

28
Q

What is multiple myeloma?

A

Cancer of plasma cells (i.e antibody producing cells)

29
Q

Where do abnormal plasma cells collect in multiple myeloma? What do they interfere with?

A

Bone marrow

Red blood cell production

30
Q

What is it that gets produced in multiple myeloma which damages the kidneys?

A

Paraprotein

31
Q

How does multiple myeloma present?

A 
Bone pain
Weakness 
Fatigue
Weight loss
Hypercalcaemia
Renal failure**
Amyloidosis 
Recurrent infections
Anaemia
32
Q

Who is at most risk of multiple myeloma?

A

Black people
Old people
Female at a younger age than males

33
Q

How do renal problems manifest in multiple myeloma?

A

AKI secondary to hypercalcaemia
Monoclonal immunoglobulin deposition disease
Cast nephropathy
Amyloidosis

34
Q

What is amyloidosis?

A

Deposition of proteins in extracellular spaces

35
Q

How can renal amyloidosis be classified?

A

Primary (AL) and secondary (AA) amyloid

36
Q

How does amyloidosis present histologically?

A

Positive congo red stain

Apple green bifringence under polarised light

37
Q

Apart from the kidneys where does amyloidosis tend to occur?

A

Heart

38
Q

How is AKI due to multiple myeloma managed?

A 
Stop nephrotoxics (NSAIDs, diuretics)
Treat hypercalcaemia 
Avoid contrast 
Chemotherapy for tumour (+/- dexamethasone)
Plasma exchange
Dialysis
39
Q

How is kidney related hypercalcaemia treated?

A

Fluids

IV pamidronate

40
Q

Which type of vasculitis affects the kidney the most? Name three of these

A

Small vessel ANCA

GPA, eGPA, microscopic polyangiitis

41
Q

Which age group typically gets vasculitis’?

A

Elderly

42
Q

How do vasculitis’ present in general?

A

Constitutional symptoms (fever, arthralgia, weight loss, etc)

43
Q

Where does GPA most commonly affect?

A

Respiratory tract

44
Q

How does GPA present?

A 
Nasal crusting
Sinusitis
Rhinorrhea
Otitis media
Ulcers
Epistaxis
45
Q

Which clinical sign may be present in GPA?

A

Saddle nose (reduced blood supply to cartilage)

46
Q

How does eGPA present?

A

Asthma (late onset)
Eosinophilia
Palpable purpura or subcutaneous nodules

47
Q

Where does eGPA most commonly affect?

A

Lungs

48
Q

What do GPA and eGPA have in common histologically?

A

Necrotising granulomatous inflammation

49
Q

Are there granulomas in microscopic polyangiitis?

A

No

50
Q

Pulmonary haemorrhages can occur in which small vessel vasculitis’? Why?

A

GPA
eGPA
Microscopic polyangiitis
Alveolar capillary involvement

51
Q

How are small vessel vasculitis’ diagnosed?

A 
Urinalysis
CRP, PV
Complement
ANCA
Biopsy of involved sites
52
Q

Which ANCAs are associated with the small vessel vasculitis’?

A

GPA - c-ANCA (cytoplasmic) & PR3

eGPA - p-ANCA (perinuclear) & MPO

53
Q

Renal involvement is most common in which two small vessel vaculitis’? How does it present?

A

GPA
Microscopic polyangiitis

Proteinuria
Haematuria
AKI
Biopsy showing segmental necrotising GN

54
Q

Crescents on renal biopsy are characteristic of what?

A

Vasculitis

55
Q

How are vasculitis’ treated?

A 
Immunosuppression (IV methylpred & cyclophosamide) 
Plasma exchange
Renal support (i.e dialysis)
56
Q

What is the cause of SLE?

A

No one knows

57
Q

What systems can be affected in SLE?

A 
Skin
Joints
Kidneys
Lungs
Serous membranes
Nerves
58
Q

Which patients most commonly get SLE?

A

Young woman
African american people
Hispanic people

59
Q

How might SLE present?

A 
Malar rash
Discoid rash
Photosensitivity 
Oral ulcers
Non-erosive arthritis 
Pluropericarditis 
Renal impairment
60
Q

Which antibodies are positive in SLE?

A

Anti-dsDNA
Anti-ANA
Anti-Sm

61
Q

What is renal disease caused by SLE called? How does it most commonly present?

A

Lupus nephritis

Proteinuria +/- haematuria

62
Q

How is lupus nephritis treated?

A

ACE/ARB

Immunosuppression (high dose steroids + immunosuppressant –> steroids + immunosuppressant)

63
Q

What are the poor prognostic features of SLE?

A 
Male
Renal involvement
Extremes of age at presentation
Anti-phospholipid syndrome
High disease activity

Year 2 (72 decks)

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