Intro to Acute Kidney Injury (AKI) Flashcards

1
Q

What is the definition of AKI?

A

AKI - Acute Kidney Injury.

  • ‘The syndrome arising from a rapidly falling GFR’

Characterised by retention of both nitrogenous (e.g. urea and creatinine) and non-nitrogenous waste products,

  • As well as disordered electrolyte, acid-base and fluid homeostasis.
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2
Q

How is AKI diagnosed?

(Physiologically speaking)

A

AKI present if:

Serum creatinine:

  • ≥26.5 μmol/l in ≤48h.
    • OR
  • rises to ≥1.5-fold from baseline in the preceding 7 days.

Urine output:

  • <0.5 ml/kg/h for 6 hours.
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3
Q

What is the volume of blood flow through the kidneys?

A

About 20% of the body’s blood is sent to the kidneys.

SV x HR = 70ml x 60 = 4,200-5,000ml per min.

(almost as much as the brain)

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4
Q

What three classifications of renal disease are there?

(and an example of each)

A

Pre-renal:

  • Hypovolemia,
  • Cardiac failure.

Renal / Intrinsic:

  • Lupus nephritis,
  • Acute interstitial nephritis.

Post-renal:

  • Papillary necrosis,
  • Tumours (prostate),
  • Kidney stones.
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5
Q

What is pre-renal kidney diease?

A

Anything related to a decrease in pressure/volume leading to a reduced supply of blood to the kidney.

  • therefore, decreased pressure at the glomerulus.
    e. g.
  • Low blood volume (e.g., dehydration),
  • Low blood pressure,
  • Heart failure (leading to cardiorenal syndrome),
  • Liver cirrhosis,
  • Local changes to the blood vessels supplying the kidney.
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6
Q

What is renal / intrinsic kidney diease?

A

Anything affecting the:

  • Glomerulus / blood vessels / tubules / kidney cells (interstitium).

E.g.

  • Glomerulonephritis,
  • Acute tubular necrosis (ATN),
  • Acute interstitial nephritis (AIN).
  • Drug Toxicity.
  • Other causes of intrinsic AKI are rhabdomyolysis and tumor lysis syndrome.
  • Certain medication classes such as calcineurin inhibitors (e.g., tacrolimus) can also directly damage the tubular cells of the kidney.
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7
Q

What is post-renal kidney diease?

A

Urine not flowing leading to a back pressure on the kidney tubular structures.

E.g.

  • Benign prostatic hyperplasia,
  • Kidney stones,
  • Obstructed urinary catheter,
  • Bladder stones,
  • Cancer:
    • Bladder, ureters, or prostate.
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8
Q

What are some main functions of the kidney?

(five are listed)

A

Clearance of waste products.

Excretion of electrolytes.

Control of water balance.

Regulation of acid-base balance.

Production of hormones.

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9
Q

What will happen if you dont produce any/small amounts of ultrafiltrate?

When does this become a life-threatening complication?

A

Will result in fluid accumation = oedema.

Becomes life-threatening in the lungs:

  • Pulmonary oedema.
    • (results in hypoxia)
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10
Q

What happens to the ECG during hyperkalaemia?

A

First sign = peaked t-waves.

As K+ increases, the QRS complex gets broader.

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11
Q

What is the emergency treatment for hyperkalaemia?

A

Insulin dextrose.

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12
Q

What is uraemia?

A

The retention of metabolic waste products:

(sulphate, urea, ammonia, creatinine, phosphate, e.t.c.)

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13
Q

What are some pathologies caused by uremia?

A

Pericarditis,

  • Retention of metabolic waste products:
    • (sulphate, urea, ammonia, creatinine, phosphate etc

Pleurisy,

Encephalopathy.

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14
Q

How does uremia cause pericarditis?

A

Pericarditis is the retention of metabolic waste products:

  • (sulphate, urea, ammonia, creatinine, phosphate etc)

The metabolic waste inflames the pericardium.

  • Chest pain but no dysfunction of the heart.

Fluid (and blood) can build up and fill the pericardium

  • (haemorrhagic) Pericardial effusion.

Is life-threatening.

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15
Q

What are the three stages of AKI?

(classified by KDIGO)

A
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16
Q

What is the first, immediate, step in managing a patient who you have identified has AKI?

A

Exclude a life-threatening complication;

If it is: correct / treat emergently.

17
Q

Generally, how would you treat (immediate management) AKI caused by:

Hypovolaemia?

Low BP?

Drug-induced?

Sepsis-induced?

A

Hypovolaemia:

  • Fluids.

Low BP:

  • Fluids and drugs.

Drug-induced:

  • Stop drugs.

Sepsis-induced:

  • Treat sepsis.
18
Q

What kind of drugs should you avoid in AKI?

A

Avoid nephrotoxic drugs.

19
Q

When should patients be given RRT?

A

When they have a life-threatening complication of AKI:

  • Life threatening pulmonary oedema.
  • Severe metabolic acidosis.
  • Severe hyperkalaemia, especially if ECG changes present.
  • Uraemic pericarditis.
  • Uraemic encephalopathy.