Azotemia Flashcards

1
Q

Definition

  • renal disease
  • renal insufficiency
  • renal failure
A

Renal disease: damage or functional impairment of kidneys
varying severity

Renal insufficiency: functional impairment not severe enough to cause azotaemia, but sufficient to cause loss of renal reserve

Renal failure: functional impairment severe enough to cause azotaemia and impairment of urine concentrating

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2
Q

Glomerular filtration rate (GFR)

A

Flow rate of filtered fluid through the kidneys

Defines the excretory function of the kidneys

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3
Q

Urinalysis

A
  • Dipstick analysis
  • Urine concentration (specific gravity measurement)
  • Sediment examination
  • Urine protein:creatinine ratio
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4
Q

Urine concentration

A
  • refractometer
  • Gold standard is osmolality
  • Measure of the number of particles in a solution
  • Influenced by the number & size of the particles
  • -> Glucosuria –> increase in specific gravity
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5
Q

Urine specific gravity

A
  • Interested in concentration of urine relative to plasma
  • Hyposthenuria – 1.000 to 1.007
  • Isosthenuria – 1.008 to 1.012
  • Minimally concentrated urine – 1.013 to 1.030
  • Hypersthenuria – 1.033 to 1.055
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6
Q

Azotaemia

A

Abnormal increase in the concentration of non-protein nitrogenous wastes in blood

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7
Q

Urea

A

Synthesised in the liver
Excreted by the kidney
Concentration of urea in renal medulla helps maintain solute gradient

Serum levels affected by:

  • Species
  • Age
  • Liver function
  • Dietary protein content (including GI bleeding)
  • Endogenous protein catabolism
  • Renal function
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8
Q

Creatinine

A
  • Synthesised by breakdown of creatine in skeletal muscle
  • Produced at constant rate
  • Depends on muscle mass
  • Excreted unchanged by kidneys

Serum concentration increased with:
- Reduced renal clearance (↓GFR)

Serum concentration decreased in:
- Reduced muscle mass

Creatinine better indicator of GFR than urea BUT relationship is not linear
Azotaemia does not develop until GFR has decreased to 25%

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9
Q

Creatinine and GFR

  • relationship
  • limitations
A

Creatinine better indicator of GFR than urea BUT relationship is not linear
Azotaemia does not develop until GFR has decreased to 25%

Limitations

  • Does not tell you why the GFR has fallen
  • Does not discriminate between:
  • Causes of azotaemia
  • Acute or chronic renal failure
  • Reversible or irreversible renal failure
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10
Q

ureamia and azotemia

A

All uraemic patients are azotaemic but not all azotaemic patients are uraemic

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11
Q

Uraemia CS

A
Inappetance
Depression
Vomiting/ Nausea
Halitosis
Diarrhoea
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12
Q

Causes of azotemia

A
  • pre-renal: inadequate blood flow
  • renal: intrinsic renal failure
  • post renal: Post-renal obstruction or rupture of urinary tract

azotemia does not equal renal disease

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13
Q

Differentiating the cause of azotemia

A

History:
- pollakiuria or stranguria (post-renal)

Clinical examination:

  • Evidence of dehydration (pre-renal +/- renal +/- post-renal)
  • Grossly enlarged bladder on palpation (post-renal)
  • Difficult or impossible to pass urinary catheter (post-renal)
  • Localised subcutaneous fluid around perineum or ventral abdomen (post-renal)
  • Free peritoneal fluid (post-renal)

Urinanalysis:

  • Specific gravity (before fluid therapy):
  • -> Hypersthenuric (pre-renal)
  • -> Remember that drugs & some non-renal illnesses can cause dehydration and pre-renal azotaemia with dilute urine
  • Urine sediment (before fluid therapy):
  • -> Active sediment with tubular casts (renal)
  • -> Haematuria (renal or post-renal)
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14
Q

Acute renal failure

  • what
  • causes
  • risk factors (3)
A

Sudden, often reversible reduction of the elimination and metabolic functions of the kidneys

Often due to a toxic or ischaemic insult

Kidneys are at high risk of damage:
- Huge blood flow
- Toxins may be secreted/reabsorbed by tubular cells
- Potential concentrating effects of toxins in urine
Play a role in biotransformation of drugs/toxins

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15
Q

Acute renal failure causes

A

x

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16
Q

Acute vs chonic renal failure

A

Acute:

  • health good until recently
  • often anuric/oliguic, sometimes polyuric
  • no weightloss
  • good coat condition
  • good BCS
  • pink MM
  • normal sized kidneys, may be painful on palpation
  • no anaemia- urine sediment contains cells, casts and debris
  • hyperkalaemia
  • metabolic acidosis

Chronic

  • months of PU/PD
  • polyuric
  • weightloss
  • poor coat
  • poor BCS
  • MM may be pale
  • small kidneys, non-painful
  • non regenerative anaemia
  • urine sediment is usually negative
17
Q

Hypoadrenocorticism (Addison’s disease)

A

Looks like ARF

Often patients will have:

  • Azotaemia (pre-renal)
  • Hyperkalaemia
  • Minimally concentrated urine
18
Q

urine output

A

Normal urine output is 1-2ml/kg/hr

Anuria – no urine production

Oliguria - 2ml/kg/hr

19
Q

Treatment

A

Need intensive care & intensive monitoring
24 hour monitoring
Close monitoring of hydration status & weight
Measurement of urine output
Monitoring of electrolytes & acid/base balance
Central venous pressure monitoring
May need peritoneal dialysis or haemodialysis

Remove inciting cause
Restore renal perfusion
Consider drugs to increase urine output
Monitor electrolytes, acid-base balance, hydration status q 6-8h or more & treat as necessary
Treat uraemic complications
Investigate underlying causes

Anuric patients are hardest to manage
very sensitive to fluid therapy

20
Q

Fluid therapy

A
  • try to minimise risk of pre renal
  • normal (0.9%) saline
  • Monitor closely for signs of overhydration
21
Q

Increasing Urine output

A

If no signs of overhydration, try mild volume expansion (3-5% of patient’s body weight)
Monitor closely

Consider diuretic administration
Frusemide or mannitol
No evidence diuretic therapy hastens recovery from ARF
No evidence that it decreases mortality 
DO NOT USE UNTIL DEHYDRATION CORRECTED