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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
Management of FSGS
- Primary: high dose glucocorticoids | - Secondary: treat underling cause and reduce proteinuria with ACE inhibitors
26
Clinical features of membranous nephropathy
- Age between 30-50 - Caucasian - Proteinuria - Oedema - Hypoalbuminaemia - Kidney failure
27
Investigation results in membranous nephropathy
- Renal biopsy: segmental scars | - Silver staining: GBM spikes
28
Prognosis of membranous nephropathy
- 1/3rd will progress to end stage renal disease - 1/3rd will remain stable - 1/3rd will resolve spontaneously
29
Management of membranous nephropathy
- High dose glucocorticoids and immunosuppressants
30
Investigation specific for amyloidosis
- Congo red staining - apple-green colour under polarised light
31
Inheritance mode of polycystic kidney disease
Autosomal dominant
32
Clinical features of adult polycystic kidney disease
- 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
Most common mutation in adult PKD
PKD1 (85%) | other 15% are PKD2
34
Diagnostic investigation for adult PKD
- 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
Management of PKD
- 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
Inheritance pattern of Alport's syndrome
X-linked
37
Clinical features of Alport's syndrome
Typically, progressive symptoms develop in the teenage years and progress to ESRD in their 20s: - Haematuria - Proteinuria - Renal failure - Sensorineural deafness - Ocular abnormalities
38
Renal biopsy result in Alport's syndrome
- Thin or thick, split and degenerating GBM
39
Management of Alport's syndrome
- ACE inhibitors | - Dialysis
40
Causes of acute interstitial nephritis
- Allergic e.g. NSAIDs, antibiotics, PPIs, mesalazine - Immune - Infective e.g. acute bacterial pyelonephritis, TB - Toxins e.g. myeloma light chains, mushrooms
41
Clinical features of acute interstitial nephritis
- 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
Investigation results in acute interstitial nephritis
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
Management of acute interstitial nephritis
- Withdrawal/treatment of precipitating factors | - High dose prednisolone
44
Causes of chronic interstitial nephritis
- 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
Clinical features of chronic interstitial nephritis
- CKD - Hypertension - Renal hypoplasia
46
Clinical features of salt-losing nephropathy
- Hypotension - Polyuria - Features of sodium and water depletion
47
Investigation results in chronic interstitial nephritis
- Non-specific urinalysis abnormalities
48
Management of chronic interstitial nephritis
- Supportive management
49
Causes of rhabdomyolysis
- Pressure - Crush injury - Ischaemic injury - Drugs e.g. statin - Extreme exercise
50
Investigation results in rhabdomyolysis
- Increased urinary myoglobin - Increased serum potassium - Increased serum phosphate - Decreased serum calcium - Increased creatinine kinase - Increased LDH
51
Management options for rhabdomyolysis
- Emergency treatment of hyperkalemia - Preventative treatment e.g. fluids - Sodium bicarbonate - Dialysis - Muscle compartment pressures and fasciotomy if required
52
Causes of renal artery stenosis
- Atherosclerosis - Fibromuscular dysplasia - Vasculitis - Thromboembolism - Aneurysms
53
Clinical features of renal artery stenosis
- Hypertension - Acute pulmonary oedema - Progressive renal failure - Deterioration in renal function with ACE inhibitors or ARBs - Clinical evidence of peripheral vascular disease
54
Features on examination when make a diagnosis of renal artery stenosis more likely
- 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
Blood test results in renal artery stenosis
- Impaired renal function - Elevated plasma renin - Hypokalemia
56
Imaging to consider in renal artery stenosis
- CT/MR angiography
57
Management of renal artery stenosis
Anti-hypertensives
58
Indications for surgical intervention (angioplasty or stenting) in renal artery stenosis
- Patients <40 - Blood pressure not controlled with anti-hypertensive medication - History of flash pulmonary oedema - Malignant hypertension - Deteriorating renal function
59
Complications of renal artery angioplasty/stenting
- Renal artery occlusion - Renal infarction - Atheroembolism
60
Clinical features of acute renal infarction
- Acute onset loin pain - Non-visible haematuria - Severe hypertension - AK and anuria (in bilateral obstruction) - Signs of widespread vascular disease
61
Investigations and results in acute renal infarction
- Bloods: Increased LDH and CRP | - CT scan
62
Management of acute renal infarction
- Mostly supportive - Anticoagulants if source identified - Stenting if presents early enough
63
Most common infective causes of HUS
- E. Coli | - Shigella dysenteriae
64
Management of HUS
- Renal replacement therapy as required
65
Clinical features of cholesterol emboli
- Renal impairment - Haematuria - Proteinuria - Eosinophilia with inflammatory features - Widespread atheromatous disease with recent intervention or surgery, or anticoagulant/thrombolytic treatment
66
Management of a cholesterol emboli
No specific management available
67
Define AKI
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
Causes of AKI
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
Investigations to consider in a patient with suspected AKI
- Routine bloods - Urinalysis - Renal US - CXR - Cultures
70
Examination/investigation results which would suggest a pre-renal cause of AKI
- Hypotension - Tachycardia - Weight loss - Dry mucous membranes - Increased skin turgor - JVP not visible - LOW urinary sodium - High urea: creatinine ratio
71
Examination/investigation results which would suggest a renal cause of AKI
- Hypertension - Oedema - Purpuric rash - Uveitis, arthritis - HIGH urinary sodium - Inappropriately dilute urine - Urinalysis: blood and protein (or none in ATN)
72
Management principles in AKI
- 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
Indications for haemodialysis in AKI
- 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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