Renal for Finals Flashcards

1
Q

What are the diagnostic criteria for acute kidney injury?

A
  • Sudden (within 1 week) rise in creatinine to 1.5x above baseline, where the baseline has been measured within 1 year
  • Oliguria (less than 0.5ml/kg/hr) for 6-12 hours
  • Anuria for more than 12 hours
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2
Q

How many stages of AKI are there?

A

3

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3
Q

What is Stage 1 AKI defined as?

A

Increase in creatinine more than 26umol/L within 48 hours OR 1.5-1.9x baseline OR urine output less than 0.5ml/kg/hr for more than 6 hours

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4
Q

What is Stage 2 AKI defined as?

A

Increase in creatinine by 2-2.9x baseline OR urine output less than 0.5ml/kg/hr for more than 12 hours

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5
Q

What is Stage 3 AKI defined as?

A

Increased in creatinine more than 3x baseline OR increase more than 354umol/L OR commencement of acute renal replacement therapy OR anuria for more than 12 hours OR urine output less than 0.3ml/kg/hr for more than 24 hours

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6
Q

True / False: Diagnosis of AKI is made using eGFR

A

False - eGFR cannot be assessed in AKI as the calculation requires a steady state of renal function. Creatinine is used as a marker of acute kidney injury instead.

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7
Q

If a patient has anuria for more than 12 hours, what stage of AKI are they in?

A

Stage 3

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8
Q

If a patient has a rise in creatinine of 2.4x their baseline, what stage of AKI do they have?

A

Stage 2

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9
Q

If a patient has a urine output of 0.4ml/kg/hr for 7 hours, what stage of AKI are they in?

A

Stage 1

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10
Q

List some drug causes of AKI

A
Metformin
ACE-Inhibitors
Aminoglycosides
Diuretics
Contrast agents
NSAIDs
Penicillamine
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11
Q

List some pre-renal causes of AKI

A
Diarrhoea
Vomiting
Sepsis
Hypotension e.g. in cardiac failure, cardiogenic shock
Haemorrhage
Dehydration
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12
Q

List some renal causes of AKI

A

Renal tubular acidosis
Glomerulonephritis
Acute interstitial nephritis
Rhabdomyolysis

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13
Q

List some post-renal causes of AKI

A

Renal or ureteric stones
BPH
Urethral stricture
Malignancy

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14
Q

How would you manage a patient with AKI?

A
  • DR ABCDE approach
  • Insert urinary catheter for accurate urine output measurement
  • fluid resuscitation if required
  • Stop nephrotoxic drugs
  • Look for a cause and treat it
  • Monitor electrolyte, acid-base balance, weight
  • Supportive management e.g. fluids
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15
Q

What investigations would you do in suspected AKI?

A
  • Fluid assessment of the patient
  • Full examination e.g. for colicky pain, haemorrhage, etc.
  • Observations: ?Tachycardia, ?hypotension, ?pyrexia
  • VBG
  • Accurate urine output recording
  • Urine dip and send for MC+S
  • Urine protein:creatinine ratio…If reduced
  • Bloods: FBC, U+E, CRP, CK, myeloma screen, autoantibodies, C3/C4, virology
  • Consider imaging of renal tract e.g. USS renal tract
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16
Q

Give 2 ways in which uraemia might present

A

Pericarditis

Encephalopathy

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17
Q

What part of the kidney do ACE-Inhibitors affect?

A

The efferent renal arteriole

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18
Q

Give 2 drugs which might be toxic to the renal tubule

A

Gentamicin

Amphoteracin

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19
Q

Do sulphonamides cause pre-renal, renal, or post-renal damage? How?

A

Post-renal - They might crystallise in the renal tubules causing obstruction

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20
Q

Give a type of drug (with examples) which might cause post-renal damage to kidneys by scarring of the ureters

A

Ergot derivatives e.g. Methylsergide (migraine) and cabergoline (Parkinson’s)…These can causes retroperitoneal fibrosis and result in scarring of the ureters

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21
Q

What is the glomerular filtration rate?

A

Volume of filtrate produced by the blood which is flowing through the glomerulus in a unit time

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22
Q

What are the stages of chronic kidney disease?

A

Stage 1 = eGFR above 90, with evidence of other renal damage
Stage 2 = eGFR 60-90, with evidence of other renal damage
Stage 3 = eGFR 30-60 ± evidence of other renal damage (Stage 3a = eGFR 45-59, stage 3b = eGFR 30-45)
Stage 4 = eGFR 15-30 ± evidence of other renal damage
Stage 5 = eGFR less than 15

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23
Q

What is the creatinine clearance? Why is it useful?

A

It is the volume of blood which is cleared of creatinine per unit time, and is a useful estimate of eGFR

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24
Q

How do you calculate creatinine clearance?

A

[ (40 x age) x weight ] / [ 72 x creatinine ] = Creatinine clearance

Multiply by 0.85 if female

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25
Q

Give 2 congenital causes of chronic kidney disease

A

Autosomal dominant polycystic kidney disease

Alport’s disease

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26
Q

List some complications of chronic kidney disease

A
Anaemia
Metabolic abnormalities: Hyperkalaemia
Hyperphosphataemia
Secondary hyperparathyroidism
Hypocalcaemia
Fluid retention - Hypertension, fluid overload
Acidosis
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27
Q

Why do patients with chronic kidney disease get anaemia?

A
  • Lack of erythropoietin production from kidneys

- Lack of absorption of iron from the gut

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28
Q

What is the treatment for anaemia in chronic kidney disease?

A

Replace iron

Replace EPO if necessary (Eprex)

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29
Q

List some key causes of chronic kidney disease

A
Hypertension
Diabetes
Drugs
Congenital e.g. ADPKD, Alport's
Glomerulonephritis
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30
Q

What is the mechanism by which phosphate is raised in chronic kidney disease?

A

The kidney is unable to excrete phosphate. In addition, phosphate stimulates PTH production, which would normally reduce the levels of phosphate, but because the kidneys cannot get rid of phosphate it builds up. PTH also stimulates phosphate release from bone via osteoclast activity, so it builds up even more.

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31
Q

What can be given to reduce phosphate levels in chronic kidney disease?

A

Phosphate binders e.g. Calcichew (also contains calcium), Sevelamir

These bind phosphate in the gut and stop it’s absorption when it is ingested in food.

Also encourage low phosphate diet e.g. avoid dairy products, legumes

32
Q

Why do patients with chronic kidney disease have hypocalcaemia?

A

The kidneys are unable to activate Vitamin D, which would normally act to absorb calcium from the gut. This means no calcium is absorbed.

NB - Calcium might be normal as PTH stimulates it’s release from bone

33
Q

Why might patients with chronic kidney disease have raised parathyroid hormone?

A

Several mechanisms:

  • Phosphate causes PTH release and there are high levels of phosphate in CKD. Normal regulation of phosphate is dysfunctional as kidneys are unable to excrete phosphate and so PTH rises further
  • Low calcium stimulated PTH release
34
Q

What might be given in chronic kidney disease to raise calcium levels?

A
  • Calcichew (also a phosphate binder)

- Alfacalcidol…a Vitamin D analogue (activated)

35
Q

True / False: Potassium is usually low in CKD

A

False - Hyperkalaemia is a common complication in CKD due to dysregulation of potassium

36
Q

Why do patients with chronic disease get acidosis?

A
  • Failure to reabsorb bicarbonate
  • Failure to acidify urine
  • Failure to excrete acidic anions
37
Q

How might you treat acidosis in a patient with chronic kidney disease?

A

Consider bicarbonate supplements

38
Q

How would you treat fluid retention and hypertension in chronic kidney disease?

A
  • Diuretics
  • Antihypertensives
  • Fluid restriction
39
Q

True / False: Polycystic kidney disease is usually bilateral

A

True

40
Q

What is the inheritance pattern of Alport’s disease?

A

X-linked dominant

41
Q

Give one feature which is classically pathagnomic of Alport’s syndrome

A

Lenticonus

42
Q

Give some features of Alport’s syndrome

A

Renal failure: Haematuria, proteinuria
Lenticonus
Sensorineural deafness
Cataracts

43
Q

What are the indications for renal replacement therapy?

A

Remember AEIOU:

  • Acidosis
  • Electrolyte imbalance e.g. persistently high K+
  • Intoxication i.e. drugs
  • Oedema refractory to treatment
  • Uraemia (symptomatic) i.e. Itching, altered cognitive function, pericarditis
44
Q

What are the drugs which might indicate the need for renal replacement therapy?

A

Remember BLAST:

  • Barbiturates
  • Lithium
  • Alcohol
  • Salicylates
  • Theophyllines
45
Q

Give 1 immunosuppressive agent used in renal transplant patients

A

Ciclosporin

46
Q

Give 2 side effects of ciclosporin

A

Gum hypertrophy

Tremor

47
Q

What is Steal Syndrome?

A

Complication of a fistula - Veins deeper to the fistula become less well perfused as blood flows preferentially through the fistula

48
Q

List some complications of a fistula

A
Bleeding
Stenosis
Aneurysm
Steal syndrome
High output cardiac failure
49
Q

Which type of renal replacement therapy is likely to be chosen in acute renal failure?

A

Haemofiltration

50
Q

What is the main complication from peritoneal dialysis to be aware of?

A

Peritonitis

51
Q

What is the triad of features in nephrotic syndrome?

A

Hypoalbuminaemia
Oedema
Proteinuria

52
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change nephropathy

53
Q

What is the most common cause of nephritic syndrome?

A

IgA nephropathy

54
Q

What do light microscopy, immunofluoroscopy and electron microscopy show in minimal change disease?

A

Light microscopy = Normal
Immunofluorescence = Normal
Electron microscopy = Podocyte effacement

55
Q

What is the treatment for minimal change disease?

A

Steroids and supportive care. Generally good response.

56
Q

Podocyte effacement is typical of which type of glomerulonephritis?

A

Minimal change disease

57
Q

Give 3 glomerulonephritides which are primarily nephrotic in nature

A

Minimal change disease
Membranous glomerulonephritis
Focal segmental glomerulonephritis

58
Q

Kimmelsteil-Wilson nodules are typical of which type of glomerulonephritis?

A

Diabetic FSGS

59
Q

Apple green birefringents on Congo red stain is typical of which type of glomerulonephritis?

A

Amyloid FSGS

60
Q

What do light microscopy, immunofluoroscopy and electron microscopy show in focal segmental glomerulonephritis?

A

Light microscopy = Thickening of basement membrane, no immune cells
Electron microscopy = Dense depositis and spikes (sub-epithelial or epithelial)
Immunofluorescence = Complement and IgG deposition

61
Q

List some associations of membranous glomerulonephritis

A

Drugs: Penicillamine, gold
Infection: HIV, Hepatitis
SLE

62
Q

Thickening of the glomerular basement membrane on light microscopy is typical of which type of glomerulonephritis?

A

Membranous glomerulonephropathy

63
Q

Neutrophils and monocytes in the glomerulus visible on light microscopy is typical of which type of glomerulonephritis?

A

Post-streptococcal glomerulonephritis

64
Q

How long after infection does IgA nephropathy and post-streptococcal glomerulonephritis typically manifest?

A

IgA nephropathy = Within days

Post-streptococcal glomerulonephritis = 2-3 weeks

65
Q

Subendothelial deposition of immune complexes visible on immunofluorescence is typical of which type of glomerulonephritis?

A

Membranoproliferative

66
Q

How can you tell the difference between membranous nephropathy and membranoproliferative GN on light microscopy?

A
Membranous = Thickened basement membrane
Membranoproliferative = Thickened basement membrane AND mesangium
67
Q

What is the appearance of membranoproliferative glomerulonephritis on immunofluorescence?

A

Subendothelial deposition of immune complexes in a linear ‘tram-track’ appearance

68
Q

Which condition is associated with anti-glomerular basement membrane antibodies?

A

Goodpasture’s

69
Q

What are the typical features of Goodpasture’s disease?

A

Haemoptysis

Renal failure

70
Q

Which conditions are associated with rapidly progressive glomerulonephritis?

A

Goodpasture’s

ANCA +ve vasculitides: Churg-Strauss, Wegerner’s, microscopic polyangiitis

71
Q

What is the best investigation for renal calculi?

A

Non-contrast CT scan

72
Q

What are the different types of renal stone?

A

Calcium oxalate
Uric acid
Infective i.e. magnesium ammonium phosphate (struvite)
Cystine

73
Q

Which type of renal stones produce a ‘stag-horn’ appearance on x-ray?

A

Struvite i.e. magnesium ammonium phosphate

74
Q

Which is the only radiolucent type of renal stone?

A

Uric acid

75
Q

What are the management options for renal stones?

A

Conservative - Small stones may require no treatment
Analgesia
Alpha blocker e.g. tamsulosin - Aids ureteric relaxation and stone passage
Extra-corporeal shockwave lithotripsy (ESWL)
Flexible ureterorenoscopy
Percutaneous nephrolithotomy
Laparoscopic / open surgery