8.15 Acute Renal Failure Flashcards

1
Q

What is the best marker for kidney function?

A

Creatinine (muscle fuel)
Look at glomerular filtration rate (GFR)

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2
Q

What is normal creatinie?

A

M: 80-100
F: 60-80

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3
Q

What to do if creatine is high in pt?

A
  • ANY increase in creatine is NB!!
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4
Q

Acute renal failure

A
  • abrupt decline in renal function
  • rise in urea & creatinine
  • reversible
  • mortality: 20% overall (acute insult to kidney) 50% ICU
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5
Q

Acute vs. Chronic

A
  • previous creatinine levels (if previously ⬆️ = chronic)
  • kidney size (Ultrasound)
  • kidney biopsy (when don’t know what caused it) chronic = show sclerosis
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6
Q

NB Etiology of ARF (Acute renal failure)

A

1. Prerenal 75%
- lack of perfusion (bloodflow)
- tubular necrosis

2. Renal of kidney itself
- bloodvessels
- glomerulus
- tubules (ATN)
- interstitium

3. Postrenal
- obstruction

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7
Q

Prerenal failure

A
  • nothing wrong with kidney
  • not being profused (Blood flow low or low BP)
  • ischemia is driver
  • progession leads to tubular necrosis
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8
Q

Renal causes of ARF

A
  • bloodvessels
  • glomerulus
  • tubules
  • interstitial

Slide 9

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9
Q

Postrenal failure

A
  • diagnosis by ultrasound
  • Renal failure if both kidneys obstructed
  • prostate
  • bladder
  • stones
  • PUJ stenosis (post urethral valves)
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10
Q

Causes of reduced renal bloodflow

A
  • true hypovolaemia (bloodloss, dehydra)
  • ⬇️ effective circulatory volume or pressure (cardiac; systemic vasodilation)
  • intrarenal vasoconstriction (ACE inhibitors / NSAID’s)
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11
Q

What happens if bloodflow is reduced to kidneys?

A

Fall in GFR
- ⬇️ urine output
- ⬆️⬆️ urea
- ⬆️ creatinine

Activation of renin-AT-aldosterone
- retention of Na+ (& water) -> concentraed urine

KIDNEYS ARE NORMAL AND RESPOND APPROPRIATELY TO REDUCED PERFUSION

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12
Q

Pathogenesis of Acute Tubular Necrosis (ATN)

A
  • Ischaemic (⬇️ renal perfusion)
  • nephrotoxic (endogenous, exogenous toxin)
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13
Q

What part of kidneys can regenerate and which can’t?

A

Tubules = can
Glomerulus = can’t

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14
Q

Nephrotoxic ATN

A

Mechanisms
- vasoconstriction
- direct tubular toxicity
- tubular obstruction

Drug induced
- NSAID’s
- Radiocosides
- Aminoglycosides

Endogenous toxin
- Myoglobin (muscle necrosis)
- Haemoglobin (haemolysis)
- AL light chains (myeloma)

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15
Q

Prerenal vs. ATN

A

Prerenal
- normal kidney that hand on to Na+ and urea
- urine normal
- serum urea:creat 1:10
- good response to saline

ATN
- damaged tubules unable to concentrate or hold back Na+
- proteinuria / haematuria / casts
- serum urea:creat 1:20

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