Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A

*a reduction in renal function following an insult to the kidneys.

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2
Q

What can the causes of AKI be divided into?

A
  • Prerenal
  • intrinsic
  • post renal
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3
Q

What are the causes of prerenal AKI?

A

Major causes of AKI is ischaemia, or lack of blood flowing to the kidneys

Examples:
>hypovolaemia secondary to diarrhoea/vomiting
>renal artery stenosis

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4
Q

What are the causes of intrinsic AKI?

A

Relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

Examples:

  • glomerulonephritis
  • acute tubular necrosis (ATN)
  • acute interstitial nephritis (AIN), respectively
  • rhabdomyolysis
  • tumour lysis syndrome
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5
Q

What are the causes of postrenal AKI?

A

Relates to problems after the kidneys. This is where there is an obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function.

Examples:

  • kidney stone in ureter or bladder
  • benign prostatic hyperplasia
  • external compression of the ureter
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6
Q

What are the risk factors for AKI?

A
  • chronic kidney disease
  • other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
  • history of acute kidney injury
  • use of drugs with nephrotoxic potential
  • use of iodinated contrast agent within past week
  • Over 65
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7
Q

What are some examples of nephrotoxic drugs?

A

DAMN

  • Diuretics
  • ACEi/ARBs/Aminoglycosides
  • Metformin
  • NSAIDs
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8
Q

What is the definition of oliguira?

A

Less than 0.5ml/kg/hr

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9
Q

What can be given to reduce the risk of an AKI for at risk patients receiving contrast?

A
  • IV fluids given before hand to reduce the risk

* Can temp stop nephrotoxic drugs

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10
Q

What are the key ways to detect a AKI?

A
  • Reduced urine output <0.5ml/kg/hr
  • Rise in molecules that the kidney usually excretes i.e. K+, urea and creatinine
  • Fluid overload
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11
Q

What is the presentation of a patient in AKI?

A
  • reduced urine output
  • pulmonary and peripheral oedema
  • arrhythmias (secondary to changes in potassium and acid-base balance)
  • features of uraemia (for example, pericarditis or encephalopathy)
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12
Q

What does U&Es return that are important in assessing kidney function?

A
  • Urea
  • K+
  • Na+
  • Creatinine
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13
Q

What are the NICE definition of an AKI?

A
  • a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
  • a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  • a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
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14
Q

What investigations should be completed in a patient with AKI? i.e. already had U&Es done

A
  • 1st: Urinalysis
  • If patient has no identifiable cause for deterioration or at risk of urinary tract obstruction they should have a renal USS within 24hrs
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15
Q

What is the management of AKI?

A

Supportive STOP AKI
*Sepsis screen

  • Toxins review (stop nephrotoxic drugs and drugs that increase in toxicity i.e. lithium, metformin and digoxin)
  • Optimise BP: fluids
*Prevent further harm
>find underlying cause and treat
>treat complications (hyperkalaemia)
>review meds
>review fluids
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16
Q

When is the input from nephrologist required in an AKI?

A

*When the cause is not known or where the AKI is severe

17
Q

When is the input from a urologist required in AKI?

A

*With suspected AKI secondary to urinary obstruction

18
Q

When is haemodialysis required for patients with AKI?

A

When a patient is not responding to medical treatment of complications i.e. hyperkalaemia, pulmonary oedema, acidosis or uraemia

19
Q

What key test can show AKI is a pre-renal uraemia vs. Acute tubular necrosis?

A
  • In prerenal uraemia - kidneys hold on to sodium to preserve volume, urine sodium <20mmol/L
  • In acute tubular necrosis urine sodium is > 40mmol/L
20
Q

What are the RIFLE classifications for AKI?

A

RISK
Increased Cr x 1.5, or GFR decreases >25%

INJURY
Increased Cr x 2 or GFR decreases >50%

FAILURE
Increased Cr x 3 or GFR decreases by >75%

LOSS
Persistent >4 weeks

END STAGE