Kidney & systemic disease Flashcards

(63 cards)

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
What is the characteristic radiological sign of fibromuscular dysplasia?
Corkscrewing of the arteries
26
How is renovascular disease managed?
BP control | Angioplasty +/- stenting
27
Which blood pressure drugs should not be given in renal artery stenosis? Which other condition should these drugs not be given in?
ACE/ARB | Fibromuscular dysplasia
28
What is multiple myeloma?
Cancer of plasma cells (i.e antibody producing cells)
29
Where do abnormal plasma cells collect in multiple myeloma? What do they interfere with?
Bone marrow | Red blood cell production
30
What is it that gets produced in multiple myeloma which damages the kidneys?
Paraprotein
31
How does multiple myeloma present?
``` Bone pain Weakness Fatigue Weight loss Hypercalcaemia Renal failure** Amyloidosis Recurrent infections Anaemia ```
32
Who is at most risk of multiple myeloma?
Black people Old people Female at a younger age than males
33
How do renal problems manifest in multiple myeloma?
AKI secondary to hypercalcaemia Monoclonal immunoglobulin deposition disease Cast nephropathy Amyloidosis
34
What is amyloidosis?
Deposition of proteins in extracellular spaces
35
How can renal amyloidosis be classified?
Primary (AL) and secondary (AA) amyloid
36
How does amyloidosis present histologically?
Positive congo red stain | Apple green bifringence under polarised light
37
Apart from the kidneys where does amyloidosis tend to occur?
Heart
38
How is AKI due to multiple myeloma managed?
``` Stop nephrotoxics (NSAIDs, diuretics) Treat hypercalcaemia Avoid contrast Chemotherapy for tumour (+/- dexamethasone) Plasma exchange Dialysis ```
39
How is kidney related hypercalcaemia treated?
Fluids | IV pamidronate
40
Which type of vasculitis affects the kidney the most? Name three of these
Small vessel ANCA | GPA, eGPA, microscopic polyangiitis
41
Which age group typically gets vasculitis'?
Elderly
42
How do vasculitis' present in general?
Constitutional symptoms (fever, arthralgia, weight loss, etc)
43
Where does GPA most commonly affect?
Respiratory tract
44
How does GPA present?
``` Nasal crusting Sinusitis Rhinorrhea Otitis media Ulcers Epistaxis ```
45
Which clinical sign may be present in GPA?
Saddle nose (reduced blood supply to cartilage)
46
How does eGPA present?
Asthma (late onset) Eosinophilia Palpable purpura or subcutaneous nodules
47
Where does eGPA most commonly affect?
Lungs
48
What do GPA and eGPA have in common histologically?
Necrotising granulomatous inflammation
49
Are there granulomas in microscopic polyangiitis?
No
50
Pulmonary haemorrhages can occur in which small vessel vasculitis'? Why?
GPA eGPA Microscopic polyangiitis Alveolar capillary involvement
51
How are small vessel vasculitis' diagnosed?
``` Urinalysis CRP, PV Complement ANCA Biopsy of involved sites ```
52
Which ANCAs are associated with the small vessel vasculitis'?
GPA - c-ANCA (cytoplasmic) & PR3 | eGPA - p-ANCA (perinuclear) & MPO
53
Renal involvement is most common in which two small vessel vaculitis'? How does it present?
GPA Microscopic polyangiitis Proteinuria Haematuria AKI Biopsy showing segmental necrotising GN
54
Crescents on renal biopsy are characteristic of what?
Vasculitis
55
How are vasculitis' treated?
``` Immunosuppression (IV methylpred & cyclophosamide) Plasma exchange Renal support (i.e dialysis) ```
56
What is the cause of SLE?
No one knows
57
What systems can be affected in SLE?
``` Skin Joints Kidneys Lungs Serous membranes Nerves ```
58
Which patients most commonly get SLE?
Young woman African american people Hispanic people
59
How might SLE present?
``` Malar rash Discoid rash Photosensitivity Oral ulcers Non-erosive arthritis Pluropericarditis Renal impairment ```
60
Which antibodies are positive in SLE?
Anti-dsDNA Anti-ANA Anti-Sm
61
What is renal disease caused by SLE called? How does it most commonly present?
Lupus nephritis | Proteinuria +/- haematuria
62
How is lupus nephritis treated?
ACE/ARB | Immunosuppression (high dose steroids + immunosuppressant --> steroids + immunosuppressant)
63
What are the poor prognostic features of SLE?
``` Male Renal involvement Extremes of age at presentation Anti-phospholipid syndrome High disease activity ```