AKI Flashcards

1
Q

Definition of AKI

A
  • An increase in serum creatine above baseline levels

- A fall in urine output less than 400-500ml per 24 hours (oliguria)

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2
Q

What are subtypes of AKI?

A
  • Pre-renal: reduced perfusion of kidneys
  • Post-renal: urinary tract obstruction
  • Renal: intrinsic damage to renal structures
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3
Q

What is auto regulatory arteriolar responses to reduced perfusion?

A

Myogenic relaxation of afferent arteriole to maintain renal blood flow and GFR

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4
Q

What are THREE effects of RAAS in response to reduced perfusion?

A
  1. Local action of angiotensin 2 differential vasoconstriction of EA and AA (assisted by prostaglandins)
  2. Increased activity of aldosterone for sodium retention to maintain cardiac filling and tonicity of extracellular water
  3. Release of ADH to concentrate urine to preserve intravascular volume
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5
Q

What restricts GFR preservation in pre-renal phase?

A
  • CKD
  • Hypertension and diabetes
  • Prostaglandin inhibitors
  • Nephrotoxic medication
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6
Q

What arteriolar diseases reduce auto regulation?

A
  • Systemic hypertension and diabetes
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7
Q

What are components of tubuloglomerular feedback?

A
  • JG cells adjacent to afferent arteriole

- Macula densa cells of thick ascending limb of loop of Henle

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8
Q

What is function of JG cells?

A

Produce renin in response to reduced renal perfusion or reduced tubular salt delivery

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9
Q

What is function of macula densa?

A

Produce adenosine in response to increased salt delivery

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10
Q

What is effect of Angiotensin 2 on glomerular pressure?

A
  • Angiotensin 2 causes vasoconstriction of AA and EA

- Prostaglandin E2 reduces vasoconstrictive action of angiotensin 2 on AA

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11
Q

What stimulates production of PGE2?

A

Angiotensin 2

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12
Q

What are 6 effects of Angiotensin 2?

A
  • Differential glomerular arteriolar vasoconstriction
  • Aldosterone production to increase salt and water retention
  • PGE2 production
  • Stimulation of ADH release
  • Increased permeability of filtration barrier in glomerulus
  • Systemic vasoconstriction
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13
Q

How does kidney turn off glomerular filtration?

A
  1. Increased sodium delivery, due to failing proximal tubular function, to macula densa
  2. Release of adenosine, which vasoconstrictor afferent arteriole to reduce glomerular capillary pressure and turn off glomerular filtration
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14
Q

What is commonest cause of ATN?

A

Reduced renal perfusion

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15
Q

What happens during ATN?

A
  • Ischaemic tubular cell death occurs

- Glomerular filtration remains turned off by adenosine

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16
Q

What does severe and sustained loss of perfusion lead to?

A

Irreversible injury to nephrons (cortical necrosis)

17
Q

What are causes of post-renal AKI?

A
  • BILATERAL obstruction of kidneys (or bladder)

- Asymmetric function (single or dominant kidney)

18
Q

What is post obstructive diuresis?

A
  • Urine outputs in excess of 500ml/hour
  • Occurs after relief of complete obstruction due to effects of obstruction on concentrating capacity of kidney
  • Usually reversible
19
Q

What are vascular causes of AKI?

A
  • Vasculitis
  • HUS
  • thrombosis
20
Q

What are glomerular causes of AKI?

A

Nephritic syndrome

21
Q

What are commonest tubular causes of AKI?

A

ATN

22
Q

What are interstitial causes of AKI?

A

Allergic interstitial nephritis

23
Q

Mechanism of ATN

A

Hypoperfusion/medication (antibiotics) → cellular damage to tubule (ATN) → failing proximal tubule → increased salt delivery to macula densa → stimulate adenosine production → vasoconstriction of AA → reduce GFR

24
Q

What is allergic interstitial nephritis?

A

Acute inflammatory allergic reaction to an allergen

25
Q

What are causes of allergic interstitial nephritis?

A
  • Antibiotics
  • NSAIDS or COX inhibitor
  • Proton pump inhibitor
26
Q

What is allergic interstitial nephritis associated with?

A
  • Rash

- Oesinophilia