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3 - Urinary > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Define acute kidney injury

A
  • Rapid drop in GFR of a patient in a short period of time

- Increase in serum creatinine, urea and decrease in urine output

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2
Q

Why is eGFR not measured for suspected AKI

A
  • eGFR taken from serum creatinine levels but creatinine change occurs a month after kidney injury has occurred
  • Takes time for creatinine to build up in the blood
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3
Q

State the 3 categories for AKI causes

A
  • Pre-renal failure
  • Intrinsic renal failure
  • Post-renal failure
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4
Q

Explain pre-renal failure

A
  • Reduced GFR due to reduced blood flow
  • No cellular damage - kidneys maximize water fluid reabsorption
    • High aldosterone and ADH release to maximize salt reabsorption
  • Responds well when given fluid
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5
Q

List possible causes or pre-renal failure

A
  • Blood not getting to kidney - renal artery occlusion, hypovolaemia, cardiac failure, sepsis (systemic vasodilation leading to hypotension)
  • NSAIDs and ACE inhibitors
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6
Q

Define acute tubular necrosis

A
  • Damage of kidney cells so cannot reabsorb salt and water, or expel excess water
  • Fluid resuscitation can lead to fluid overload
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7
Q

What is intrinsic renal failure commonly caused by

A

Ischaemia, nephrotoxins, sepsis

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8
Q

Which area of the kidney is greatest affected by ischaemia

A
  • Cells with the highest metabolic demand are affected the most
  • Proximal tubule most affected as most reabsorption and most energy demand
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9
Q

Give examples of how nephrotoxins can cause intrinsic renal failure

A
  • Causes direct cell damage
    • Eg. Myoglobin, bilirubin, drugs, poisons, radiography contrast
  • Rhabdomyolysis - due to muscle necrosis and release of myoglobin
    • Can be due to injuries, drugs
      • High creatine kinase levels in blood and ‘coca cola’ urine colour
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10
Q

Explain how thrombotic microangiopathy causes AKI

A
  • Causes ischaemia - intrinsic renal failure
  • Endothelial damage leads to platelet thrombi which causes partial obstruction of small arterioles
  • Red blood cells become damaged and can further occlude arterioles
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11
Q

Explain how acute interstitial nephritis causes AKI

A
  • Toxin induced, infections - sepsis

- Due to inflammatory response of the body

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12
Q

State the most common causes of AKI

A

Dehydration, hypotension

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13
Q

Differentiate between pre-renal and acute tubular necrosis

A
  • Pre-renal may lead to acute tubular necrosis if untreated
  • In acute tubular necrosis, kidney unresponsive to IV fluid - may lead to fluid overload
  • In pre-renal, osmolality is high as kidney able to reabsorb salts (>500 mOsm/kg)
    • In ATN, salts and water not reabsorbed so low osmolality (<250 mOsm/kg)
    • Not accurate for elderly patients or patients on diuretics
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14
Q

Describe investigations for AKI

A
  • Urinalysis - urine dipstick - blood, protein, leucocytes
    • High blood or protein present suggests intrinsic renal disease
  • Culture urine if dipstick positive
  • Blood test - high urea and creatinine in AKI
  • Ultrasound scan to look for obstruction
  • Chest x-ray - fluid overload or infection
  • Kidney biopsy - used when pre-renal and post-renal AKI ruled out
  • Urine output - oliguric (low urine production) suggests a more serious injury than non-oliguric
    - Could be damaged filtration (low GFR), obstruction
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15
Q

Outline what to look for in blood tests for suspected AKI

A
  • High urea and creatinine in AKI
  • Hyperkalaemia - low filtration (pre-renal), decreased secretion due to decreased Na reabsorption (intrinsic), ACE inhibitors or ENaC blockers
    • Calcium gluconate should be give to prevent arrhythmia
  • Hyponatraemia - decreased reabsorption (intrinsic)
  • Metabolic acidosis - decreased bicarbonate reabsorption (intrinsic), also leads to hyperkalaemia as cells exchange H for K
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16
Q

Describe treatment measures for AKI

A
  • Pre-renal treatment involves giving fluid
    • Need to monitor urine output and signs of oedema
  • Acute tubular necrosis involves supportive treatment - maintaining kidney perfusion, avoiding nephrotoxins
  • Give calcium gluconate and stop K-sparing diuretics (ACEi) to treat hyperkalaemia
  • Dialysis is given when kidney cannot adequately secrete salts and maintain acid-base balance
17
Q

Describe the renal response to decreased renal perfusion

A
  • RAAS system activated to cause efferent vasoconstriction through angiotensin II
  • Prostaglandins released to dilate afferent arterioles to maintain GFR
18
Q

Describe how problems in renal response to reduced perfusion leads to AKI

A
  • Beyond the ability to auto-regulate, AKI occurs
    • Maximum auto-regulation occurs at about 80mmHg
  • ACE inhibitors and non-steroidal medications lead to significant GFR drop as prostaglandin and angiotensin II effect on afferent and efferent arterioles are compromised
    • Should not be taken with kidney injury

3 - Urinary (17 decks)

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