Acute Kidney Injury Flashcards

(63 cards)

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
What finding tends to indicate a glomerular problem?
Proteinuria
26
What drug classes can possibly cause interstitial nephritis?
Anti-inflammatories Protein pump inhibitors Antibiotics
27
What is the most common cause of intrinsic AKI?
ATN
28
What is ATN?
Usually because of acute event, either - Ischaemic - Toxic Oliguria not invariable > don't rely too much on urine output
29
What is happening at a cellular level in ATN?
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
What are the phases of ATN?
Initiation Maintenance Recovery
31
Does the serum creatinine level indicate GFR?
Not when it's changing, especially if it's increasing Best to assume that GFR = 0 - Helps appreciate seriousness of AKI
32
What is the pathophysiology of ATN?
Hypoperfusion > reperfusion to vascular network where there's been micro-vessel thrombosis and occlusion > further inflammation > reperfusion injury
33
What happens in the initiation phase of ATN?
Acute decrease in GFR to low-very low levels | Increase in serum creatinine and urea
34
What happens in the maintenance phase of ATN?
Sustained reduction in GFR | Creatinine and urea continue to rise
35
What happens in the recovery phase of ATN?
Tubular function restores with increase in urine volume - If oliguria present Gradual decrease in creatinine and urea
36
How long can recovery take after ATN?
2-6 weeks | Risk of chronic damage
37
How do you determine whether renal impairment is acute or chronic?
Lab values don't discriminate between acute and chronic disease Oliguria supports acute renal failure
38
What are the clues that support a chronic disease process in the kidneys?
``` Pre-existing illness - Diabetes - Hypertension - Age - Vascular disease Previous serum creatinine measurements Small, echogenic kidneys by ultrasound ```
39
What suggests that the cause is an obstruction rather than AKI?
Often complete anuria May have palpable bladder on examination Renal ultrasound shows bilateral hydronephrosis
40
How do you assess a patient's volume status?
``` History - Thirst - Lightheaded/dizziness - Cramping Examination - If can't see JVP lying down, probably very fluid deplete - Postural hypotension - Urinary concentration indices ```
41
How do you determine whether there's evidence of other intrinsic renal disease apart from ATN?
Clues from history and exam | Urinalysis, including microscopy
42
How do you determine whether a major vascular occlusion has occurred?
History of vascular disease Renal asymmetry on ultrasound Loin pain with macro haematuria Complete anuria
43
What is the treatment for AKI?
Facilitating renal repair | Very little available at present
44
What are the risk factors for developing AKI?
``` Elderly Chronic kidney disease Cardiac failure Liver disease Diabetes Vascular disease Background nephrotoxic medications ```
45
What acute insults over background morbidity may cause AKI?
Sepsis and hypoperfusion Toxicity Obstruction Parenchymal kidney disease
46
How do you prevent AKI?
Monitor patient Maintain circulation Minimise kidney insults Manage acute illness
47
How do you recognise AKI?
5x increase from most recent baseline creatinine OR | 6 hours oliguria
48
How is AKI monitored?
Discontinue offending agents and nephrotoxins Assessment of volume status Measure urea, creatinine, electrolytes, and venous bicarbonate daily while creatinine rising
49
What is the relationship between volume status and outcomes of AKI?
Volume overload associated with poorer outcomes
50
What is the mnemonic for the causes of AKI?
``` S = sepsis and hypoperfusion T = toxicity O = obstruction P = parenchymal disease ```
51
What are the investigations for AKI?
``` Urine dipstick Urine PCR Renal ultrasound LFTs CRP CK Platelet count ```
52
What is oliguric renal failure?
Urine output less than required to maintain solute balance | Less than 400 mL/24 hours
53
What is anuric renal failure?
Less than 100 mL/24 hours | Less common
54
What are the possible acute metabolic complications of AKI?
``` Volume overload Hyperkalaemia Metabolic acidosis Hypocalcaemia Infections Nutrition ```
55
How do you treat volume overload?
Salt and water restriction Diuretics - Give big dose first, because if they don't respond, escalate to dialysis
56
How do you treat hyperkalaemia?
``` Restrict K intake IV glucose and insulin Kayexalate Calcium gluconate Acute dialysis ```
57
How do you treat metabolic acidosis?
Sodium bicarbonate | Dialysis
58
How do you treat hypocalcaemia?
Calcium carbonate | Calcium gluconate
59
What is peritoneal dialysis?
Dialysate infused into peritoneal cavity Left to dwell for equilibration of solutes and fluids Used dialysate discarded
60
Describe haemodialysis
``` Solutes removed by diffusion Fast Not always well tolerated Small molecules removed Clearance of drugs variable Requires dialysis expertise ```
61
Describe haemofiltration
``` Solute removed by convection Slow Usually well tolerated Medium sized molecules removed Clearance of most drugs More expensive, in ICU ```
62
Which form of dialysis is better?
No evidence that one form better than other
63
What often dictates choice of the dialysis used?
Clinical status of patient Available resources Physician expertise