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Year 5 > Renal > Flashcards

Renal Flashcards

1
Q

Risk factors for diabetic nephropathy

A
  • Poor diabetic control
  • Long duration of diabetes
  • Presence of other microvascular complications
  • Ethnicity
  • Family history
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2
Q

Management of diabetic nephropathy

A
  • Good glycaemic control
  • Blood pressure control - ACE inhibitors + ARBs
  • Dietary changes e.g. weight loss
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3
Q

Clinical features of IgA nephropathy

A
  • Young men typically affected
  • Flares triggered by URTIs - usually 1-2 days after symptoms
  • Haematuria
  • Loin pain
  • Oedema in the hands and feet
  • Dark urine
  • Hypertension
  • Henoch-Schonlein purpura
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4
Q

Investigation results in IgA nephropathy

A
  • Increased mesangial matrix and cells

- IgA deposition in the epithelium

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5
Q

Management of IgA nephropathy

A
  • Blood pressure control with ACE inhibitors
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6
Q

Clinical features of post-streptococcal glomerulonephritis

A
  • Symptoms occur 10-14 days after streptococcal infection (e.g. strep throat, skin infection)
  • Most commonly affects children and young adults
  • Haematuria
  • Oliguria
  • Oedema
  • Hypertension
  • Fluid retention
  • Malaise
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7
Q

Investigation results in post-strep GN

A
  • Urine microscopy: Red cell casts and dysmorphic red cells
  • Bloods: positive Anti-Streptolysin test, low C3 and C4 levels
  • Renal biopsy: cresenteric lesions with diffuse proliferation of cells and immune deposits
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8
Q

Management of post-strep GN

A
  • Usually none required

- Can provide supportive management

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9
Q

Clinical features of small vessel vasculitis

A
  • Typically affects middle-aged people
  • Typically affects Caucasians
  • Visible haematuria
  • Foamy urine
  • Hypertension
  • Decreased kidney function
  • Other symptoms based on body systems affected
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10
Q

Management of small vessel vasculitis

A
  • Corticosteroids
  • Cyclophosphamide
  • Rituximab
  • Plasmapheresis
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11
Q

Clinical features of Anti-GBM/Goodpasture’s disease

A
  • Haematuria +/- proteinuria
  • Lung haemorrhage
  • Systemic symptoms e.g. weight loss, fever, malaise
  • Arthralgia
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12
Q

Investigation results in anti-GBM disease

A
  • Urine microscopy: characteristic red cell casts and dysmorphic red cells
  • Anti-GBM antibody present
  • Renal biopsy: cresenteric nephritis
  • EM: linear IgG deposits on the GBM
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13
Q

Management of anti-GBM disease

A
  • Glucocorticoids
  • Cyclophosphamide
  • Plasma exchange
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14
Q

Clinical features of Henoch-Schonlein purpura

A
  • Most commonly affects children
  • Characteristic petechial rash on the buttocks and lower legs
  • Abdominal pain
  • Arthralgia
  • Renal disease - haematuria +/- proteinuria
  • Often preceded by an infection
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15
Q

Investigation results in Henoch-Schonlein purpura

A
  • Renal biopsy: mesangial IGA deposition that are indistinguishable from IgA nephropathy
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16
Q

Causes of nephritic syndrome

A
  • IgA nephropathy
  • Post-streptococcal glomerulonephritis
  • Small vessel vasculitis
  • Anti-GBM disease
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17
Q

Causes of nephrotic syndrome

A
  • Minimal Change Disease
  • FSGS
  • Membranous nephropathy
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18
Q

Triad of symptoms seen in nephrotic syndrome

A
  • Oedema
  • Proteinuria
  • Hypoalbuminaemia
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19
Q

Clinical features of minimal change disease

A
  • Typically affects children
  • Proteinuria
  • Widespread oedema e.g. peri-orbital
  • Impaired kidney function
  • Hypoalbuminaemia
  • Associated with atopy, drugs (e.g. NSAIDs), haematological malignancies
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20
Q

Investigation results in minimal change disease

A
  • Renal biopsy: normal

- EM: fusion of foot processes

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21
Q

Management of minimal change disease

A
  • High-dose corticosteroids e.g. 6 weeks PO prednisolone
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22
Q

Causes of secondary FSGS

A
  • Healing of previous local glomerular injury e.g. HUS, cholesterol embolism, vasculitis
  • HIV
  • Sickle cell disease
  • Heroin
  • Morbid obesity
  • Chronic hypertension
  • Renal disease
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23
Q

Clinical features of FSGS

A
  • Can occur in any age group
  • More common in people of West African descent
  • Proteinuria
  • Oedema
  • Hypoalbuminaemia
  • Hyperlipidaemia
  • Kidney failure
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24
Q

Investigation results in FSGS

A
  • Renal biopsy: partial sclerosis seen in some glomeruli. May stain positive for C3 and IgM deposits on immunofluorescence.
  • EM: podocyte foot process fusion
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25
Q

Management of FSGS

A
  • Primary: high dose glucocorticoids

- Secondary: treat underling cause and reduce proteinuria with ACE inhibitors

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26
Q

Clinical features of membranous nephropathy

A
  • Age between 30-50
  • Caucasian
  • Proteinuria
  • Oedema
  • Hypoalbuminaemia
  • Kidney failure
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27
Q

Investigation results in membranous nephropathy

A
  • Renal biopsy: segmental scars

- Silver staining: GBM spikes

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28
Q

Prognosis of membranous nephropathy

A
  • 1/3rd will progress to end stage renal disease
  • 1/3rd will remain stable
  • 1/3rd will resolve spontaneously
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29
Q

Management of membranous nephropathy

A
  • High dose glucocorticoids and immunosuppressants
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30
Q

Investigation specific for amyloidosis

A
  • Congo red staining - apple-green colour under polarised light
31
Q

Inheritance mode of polycystic kidney disease

A

Autosomal dominant

32
Q

Clinical features of adult polycystic kidney disease

A
  • Asymptomatic
  • Hypertension
  • Haematuria
  • Abdominal pain
  • Uni- or bilateral palpable kidneys
  • Hepatic cysts
  • Increased risk of subarachnoid haemorrhage
  • Increased risk of renal stones
  • Increased risk of UTIs
33
Q

Most common mutation in adult PKD

A

PKD1 (85%)

other 15% are PKD2

34
Q

Diagnostic investigation for adult PKD

A
  • Renal US, using the following criteria:
    15-39: at least 3 uni or bilateral cysts
    40-59: at least 2 cysts in each kidney
    60+: at least 4 cysts in each kidney
35
Q

Management of PKD

A
  • Hypertension control with ACE inhibitors or ARBs
  • Dialysis
  • Renal transplant
  • ADH receptor antagonists (Tolvaptan) used to slow rate of cyst growth and eGFR loss
36
Q

Inheritance pattern of Alport’s syndrome

A

X-linked

37
Q

Clinical features of Alport’s syndrome

A

Typically, progressive symptoms develop in the teenage years and progress to ESRD in their 20s:

  • Haematuria
  • Proteinuria
  • Renal failure
  • Sensorineural deafness
  • Ocular abnormalities
38
Q

Renal biopsy result in Alport’s syndrome

A
  • Thin or thick, split and degenerating GBM
39
Q

Management of Alport’s syndrome

A
  • ACE inhibitors

- Dialysis

40
Q

Causes of acute interstitial nephritis

A
  • Allergic e.g. NSAIDs, antibiotics, PPIs, mesalazine
  • Immune
  • Infective e.g. acute bacterial pyelonephritis, TB
  • Toxins e.g. myeloma light chains, mushrooms
41
Q

Clinical features of acute interstitial nephritis

A
  • Electrolyte abnormalities
  • Moderate proteinuria
  • Varying degrees of renal impairment
  • Preserved urinary output e.g. polyuria, nocturia
  • May have signs of a generalised hypersensitivity reaction e.g. fever, rash
42
Q

Investigation results in acute interstitial nephritis

A

Urine dipstick:

  • No/minimal protein
  • No/minimal blood
  • White cells and white cell casts

Bloods:
- Raised eosinophil count

Renal biopsy:
- Acute inflammation with infiltration of polymorphonuclear leucocytes and lymphocytes (+/- eosinophils) +/- granulomas

43
Q

Management of acute interstitial nephritis

A
  • Withdrawal/treatment of precipitating factors

- High dose prednisolone

44
Q

Causes of chronic interstitial nephritis

A
  • AIN
  • Glomerulonephritis
  • Immune/inflammatory disorders e.g. sarcoidosis, SLE, Sjogren’s syndrome
  • Toxins e.g. lead
  • Drugs e.g. Lithium, cyclosporin
  • Severe pyelonephritis
  • Congenital abnormalities e.g. VUR
  • Metabolic disorders e.g. calcium phosphate crystallisation, hypokalemia, hyperoxaluria
45
Q

Clinical features of chronic interstitial nephritis

A
  • CKD
  • Hypertension
  • Renal hypoplasia
46
Q

Clinical features of salt-losing nephropathy

A
  • Hypotension
  • Polyuria
  • Features of sodium and water depletion
47
Q

Investigation results in chronic interstitial nephritis

A
  • Non-specific urinalysis abnormalities
48
Q

Management of chronic interstitial nephritis

A
  • Supportive management
49
Q

Causes of rhabdomyolysis

A
  • Pressure
  • Crush injury
  • Ischaemic injury
  • Drugs e.g. statin
  • Extreme exercise
50
Q

Investigation results in rhabdomyolysis

A
  • Increased urinary myoglobin
  • Increased serum potassium
  • Increased serum phosphate
  • Decreased serum calcium
  • Increased creatinine kinase
  • Increased LDH
51
Q

Management options for rhabdomyolysis

A
  • Emergency treatment of hyperkalemia
  • Preventative treatment e.g. fluids
  • Sodium bicarbonate
  • Dialysis
  • Muscle compartment pressures and fasciotomy if required
52
Q

Causes of renal artery stenosis

A
  • Atherosclerosis
  • Fibromuscular dysplasia
  • Vasculitis
  • Thromboembolism
  • Aneurysms
53
Q

Clinical features of renal artery stenosis

A
  • Hypertension
  • Acute pulmonary oedema
  • Progressive renal failure
  • Deterioration in renal function with ACE inhibitors or ARBs
  • Clinical evidence of peripheral vascular disease
54
Q

Features on examination when make a diagnosis of renal artery stenosis more likely

A
  • Severe, recent onset or difficult to control hypertension
  • Asymmetrical kidneys on US
  • Recurrent flash pulmonary oedema
  • Lower limb peripheral vascular disease present
  • Renal function deteriorates with ACE inhibitors or ARBs
55
Q

Blood test results in renal artery stenosis

A
  • Impaired renal function
  • Elevated plasma renin
  • Hypokalemia
56
Q

Imaging to consider in renal artery stenosis

A
  • CT/MR angiography
57
Q

Management of renal artery stenosis

A

Anti-hypertensives

58
Q

Indications for surgical intervention (angioplasty or stenting) in renal artery stenosis

A
  • Patients <40
  • Blood pressure not controlled with anti-hypertensive medication
  • History of flash pulmonary oedema
  • Malignant hypertension
  • Deteriorating renal function
59
Q

Complications of renal artery angioplasty/stenting

A
  • Renal artery occlusion
  • Renal infarction
  • Atheroembolism
60
Q

Clinical features of acute renal infarction

A
  • Acute onset loin pain
  • Non-visible haematuria
  • Severe hypertension
  • AK and anuria (in bilateral obstruction)
  • Signs of widespread vascular disease
61
Q

Investigations and results in acute renal infarction

A
  • Bloods: Increased LDH and CRP

- CT scan

62
Q

Management of acute renal infarction

A
  • Mostly supportive
  • Anticoagulants if source identified
  • Stenting if presents early enough
63
Q

Most common infective causes of HUS

A
  • E. Coli

- Shigella dysenteriae

64
Q

Management of HUS

A
  • Renal replacement therapy as required
65
Q

Clinical features of cholesterol emboli

A
  • Renal impairment
  • Haematuria
  • Proteinuria
  • Eosinophilia with inflammatory features
  • Widespread atheromatous disease with recent intervention or surgery, or anticoagulant/thrombolytic treatment
66
Q

Management of a cholesterol emboli

A

No specific management available

67
Q

Define AKI

A

Increase in serum creatinine >26.5 within 48 hours
OR
Increase in >1.5x baseline within 7 days
OR
Decrease in urine volume <0.5ml/kg/hr for >6 hours

68
Q

Causes of AKI

A

Pre-renal:

  • Hypotension
  • Sepsis
  • Hypovolaemia e.g. vomiting, diarrhoea, burns, haemorrhage
  • Dehydration
  • Organ failure
  • Drugs e.g. ACE inhibitors, NSAIDs
  • Liver disease
  • Cardiac failure

Renal:

  • Glomerulonephritis
  • Interstitial nephritis
  • Acute tubular necrosis (from prolonged pre-renal causes)
  • CKD
  • Renovascular disease

Post-renal:

  • Obstruction
  • Neurological conditions
  • Intra-renal cysts
69
Q

Investigations to consider in a patient with suspected AKI

A
  • Routine bloods
  • Urinalysis
  • Renal US
  • CXR
  • Cultures
70
Q

Examination/investigation results which would suggest a pre-renal cause of AKI

A
  • Hypotension
  • Tachycardia
  • Weight loss
  • Dry mucous membranes
  • Increased skin turgor
  • JVP not visible
  • LOW urinary sodium
  • High urea: creatinine ratio
71
Q

Examination/investigation results which would suggest a renal cause of AKI

A
  • Hypertension
  • Oedema
  • Purpuric rash
  • Uveitis, arthritis
  • HIGH urinary sodium
  • Inappropriately dilute urine
  • Urinalysis: blood and protein (or none in ATN)
72
Q

Management principles in AKI

A
  • Control of fluid intake - just replace predicted losses
  • Monitor and correct hypokalemia
    1) Immediate ECG
    2) IV calcium gluconate
    3) Inhaled salbutamol, IV glucose + IV insulin, IV sodium bicarbonate
    4) IV furosemide and normal saline
  • Monitor for and correct acidosis - sodium bicarbonate
  • Monitor for and treat pulmonary oedema - dialysis
  • STOP ACE inhibitors and NSAIDs
  • Treat primary cause
  • Haemodialysis if indicated
73
Q

Indications for haemodialysis in AKI

A
  • Pulmonary oedema (URGENT)
  • Severe hyperkalemia despite medical management
  • Symptomatic or poor biochemical results
  • Pericarditis
  • Need for high fluid intakes during oliguria.

Year 5 (9 decks)

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