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MD2 Foundation > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What are the consequences of acute kidney injury (AKI)?

A 
Acute metabolic complications
- Hyperkalaemia
Acute cardiovascular complications
- Pulmonary oedema
Prolonged hospitalisation
Patient death common
End-stage kidney disease (ESKD) uncommon
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2
Q

What is AKI?

A

No validated biomarker for immediate renal injury
Increased by 25 umol/L in creatinine
- Anything more than that, is more severe increase

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3
Q

What are the main physiological roles of the kidneys in the normal state?

A

Fluid balance
Excretion of waste products
Acid/base balance
Hormone production

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4
Q

How does kidney disease affect fluid balance?

A

Na/water imbalance

  • Inability to excrete fluid lode OR
  • Inability to conserve Na and water
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5
Q

How does kidney disease affect excretion of waste products?

A

Accumulation of solutes and waste products

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6
Q

How does kidney disease affect acid/base balance?

A

Accumulation of acids

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7
Q

How does kidney disease affect hormone production?

A

Abnormalities in function

  • Anaemia
  • Bone disease
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8
Q

Is loss of urine output in AKI invariable?

A

No

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9
Q

Why aren’t accumulation of solutes, waste products, and acids immediately abnormal in AKI?

A

Because time dependent

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10
Q

What are the three categories of causes of AKI?

A 
Pre-renal = sudden and severe drop in blood pressure/interruption to blood flow to kidneys
Intra-renal = direct damage to kidneys by inflammation, toxins, drugs, infection, or prolonged reduced blood supply
Post-renal = sudden obstruction due to enlarged prostate, kidney stones, bladder tumour, or injury
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11
Q

What is active urine sediment?

A

Blood and protein in urine dipstick

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12
Q

Is intrinsic renal failure common?

A

Other than due to acute tubular necrosis (ATN), no

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13
Q

What is the commonest cause of post-renal AKI in women?

A

Cervical carcinoma

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14
Q

What is the commonest cause of post-renal AKI in men?

A

Benign prostatic hypertrophy

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15
Q

What structure does prostatic carcinoma tend to block, and why?

A

Blocks ureters rather than urethra, because tends to grow behind bladder

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16
Q

What stages of AKI do pre-renal causes correspond to?

A

Stage I-II early AKI

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17
Q

What maintains blood pressure in pre-renal AKI?

A

CNS sympathetic outflow > stimulates RAAS

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18
Q

What mediates salt and water retention in pre-renal AKI?

A

Anti-diuretic hormone (ADH) and aldosterone

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19
Q

What happens to the urinary concentration capacity in pre-renal AKI?

A

Intact

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20
Q

Is pre-renal AKI reversible, and if so, how?

A

Yes, reversible by prompt restoration of renal perfusion

But prolonged hypo-perfusion causes renal decompensation

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21
Q

What happens in renal decompensation as a result of prolonged hypo-perfusion?

A

Excessive SNS and RAAS > ischaemic injury

Dysautoregulation with concomitant NSAID and ACE inhibitor

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22
Q

Is intrinsic AKI reversible?

A

Not readily

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23
Q

What are the possible pathologies of intrinsic AKI?

A 
Tubular injury
- Common
- Ischaemia/prolonged hypoperfusion = ATN
- Toxins
Interstitial nephritis
- Common
- Drugs
- Infection
- Infiltration
Glomeruli
- Uncommon
- Inflammation = glomerulonephritis
- Thrombosis
Vascular disease
- Uncommon
- Inflammation = vasculitis
- Occlusion
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24
Q

Which part of the nephron is most susceptible to ischaemia?

A

Thick ascending loop of Henle

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25
Q

What finding tends to indicate a glomerular problem?

A

Proteinuria

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26
Q

What drug classes can possibly cause interstitial nephritis?

A

Anti-inflammatories
Protein pump inhibitors
Antibiotics

27
Q

What is the most common cause of intrinsic AKI?

A

ATN

28
Q

What is ATN?

A

Usually because of acute event, either
- Ischaemic
- Toxic
Oliguria not invariable > don’t rely too much on urine output

29
Q

What is happening at a cellular level in ATN?

A

Ischaemic depletion of ATP > release of ROS and apoptosis
Cell desquamation > obstructive cast > back-leak of tubular fluid
Reversible after regeneration of tubular endothelial cells

30
Q

What are the phases of ATN?

A

Initiation
Maintenance
Recovery

31
Q

Does the serum creatinine level indicate GFR?

A

Not when it’s changing, especially if it’s increasing
Best to assume that GFR = 0
- Helps appreciate seriousness of AKI

32
Q

What is the pathophysiology of ATN?

A

Hypoperfusion > reperfusion to vascular network where there’s been micro-vessel thrombosis and occlusion > further inflammation > reperfusion injury

33
Q

What happens in the initiation phase of ATN?

A

Acute decrease in GFR to low-very low levels

Increase in serum creatinine and urea

34
Q

What happens in the maintenance phase of ATN?

A

Sustained reduction in GFR

Creatinine and urea continue to rise

35
Q

What happens in the recovery phase of ATN?

A

Tubular function restores with increase in urine volume
- If oliguria present
Gradual decrease in creatinine and urea

36
Q

How long can recovery take after ATN?

A

2-6 weeks

Risk of chronic damage

37
Q

How do you determine whether renal impairment is acute or chronic?

A

Lab values don’t discriminate between acute and chronic disease
Oliguria supports acute renal failure

38
Q

What are the clues that support a chronic disease process in the kidneys?

A 
Pre-existing illness
- Diabetes
- Hypertension
- Age
- Vascular disease
Previous serum creatinine measurements
Small, echogenic kidneys by ultrasound
39
Q

What suggests that the cause is an obstruction rather than AKI?

A

Often complete anuria
May have palpable bladder on examination
Renal ultrasound shows bilateral hydronephrosis

40
Q

How do you assess a patient’s volume status?

A 
History
- Thirst
- Lightheaded/dizziness
- Cramping
Examination
- If can't see JVP lying down, probably very fluid deplete
- Postural hypotension
- Urinary concentration indices
41
Q

How do you determine whether there’s evidence of other intrinsic renal disease apart from ATN?

A

Clues from history and exam

Urinalysis, including microscopy

42
Q

How do you determine whether a major vascular occlusion has occurred?

A

History of vascular disease
Renal asymmetry on ultrasound
Loin pain with macro haematuria
Complete anuria

43
Q

What is the treatment for AKI?

A

Facilitating renal repair

Very little available at present

44
Q

What are the risk factors for developing AKI?

A 
Elderly
Chronic kidney disease
Cardiac failure
Liver disease
Diabetes
Vascular disease
Background nephrotoxic medications
45
Q

What acute insults over background morbidity may cause AKI?

A

Sepsis and hypoperfusion
Toxicity
Obstruction
Parenchymal kidney disease

46
Q

How do you prevent AKI?

A

Monitor patient
Maintain circulation
Minimise kidney insults
Manage acute illness

47
Q

How do you recognise AKI?

A

5x increase from most recent baseline creatinine OR

6 hours oliguria

48
Q

How is AKI monitored?

A

Discontinue offending agents and nephrotoxins
Assessment of volume status
Measure urea, creatinine, electrolytes, and venous bicarbonate daily while creatinine rising

49
Q

What is the relationship between volume status and outcomes of AKI?

A

Volume overload associated with poorer outcomes

50
Q

What is the mnemonic for the causes of AKI?

A 
S = sepsis and hypoperfusion
T = toxicity
O = obstruction
P = parenchymal disease
51
Q

What are the investigations for AKI?

A 
Urine dipstick
Urine PCR
Renal ultrasound
LFTs
CRP
CK
Platelet count
52
Q

What is oliguric renal failure?

A

Urine output less than required to maintain solute balance

Less than 400 mL/24 hours

53
Q

What is anuric renal failure?

A

Less than 100 mL/24 hours

Less common

54
Q

What are the possible acute metabolic complications of AKI?

A 
Volume overload
Hyperkalaemia
Metabolic acidosis
Hypocalcaemia
Infections
Nutrition
55
Q

How do you treat volume overload?

A

Salt and water restriction
Diuretics
- Give big dose first, because if they don’t respond, escalate to dialysis

56
Q

How do you treat hyperkalaemia?

A 
Restrict K intake
IV glucose and insulin
Kayexalate
Calcium gluconate
Acute dialysis
57
Q

How do you treat metabolic acidosis?

A

Sodium bicarbonate

Dialysis

58
Q

How do you treat hypocalcaemia?

A

Calcium carbonate

Calcium gluconate

59
Q

What is peritoneal dialysis?

A

Dialysate infused into peritoneal cavity
Left to dwell for equilibration of solutes and fluids
Used dialysate discarded

60
Q

Describe haemodialysis

A 
Solutes removed by diffusion
Fast
Not always well tolerated
Small molecules removed
Clearance of drugs variable
Requires dialysis expertise
61
Q

Describe haemofiltration

A 
Solute removed by convection
Slow
Usually well tolerated
Medium sized molecules removed
Clearance of most drugs
More expensive, in ICU
62
Q

Which form of dialysis is better?

A

No evidence that one form better than other

63
Q

What often dictates choice of the dialysis used?

A

Clinical status of patient
Available resources
Physician expertise

MD2 Foundation (42 decks)

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