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MODULE 17 - Urinary, Endocrine and Oncological Disease > PATHOLOGY - Azotaemia and Acute Kidney Injury (AKI) > Flashcards

PATHOLOGY - Azotaemia and Acute Kidney Injury (AKI) Flashcards

1
Q

What are the functions of the kidney?

A

Filtration of blood and excretion of metabolic waste
Acid-base balance
Volume regulation
Electrolyte regulation
Blood pressure regulation
Produces erythropoietin

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2
Q

What is the general clinical presentation of renal disease?

A

Polyuria, polydipsia (PUPD)
Haematuria
Inappetence
Weight loss
Lethargy
Gastrointestinal signs (vomiting, nausea, diarrhoea)
Ascites
Subcutaneous oedema
Abdominal pain

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3
Q

What is renal disease?

A

Renal disease is the term used to describe damage or functional impairment of the kidneys, which can have varying severity

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4
Q

What is renal insufficiency?

A

Renal insufficiency is the term used to describe functional impairement of the kidneys that is not severe enough to cause azotaemia

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5
Q

What is renal failure?

A

Renal failure is the term used to describe functional impairement of the kidneys that is severe enough to cause azotaemia and often impair the kidneys ability to concentrate urine

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6
Q

What is azotaemia?

A

Azotaemia is an abnormal increase in non-protein nitrgenous waste (urea and creatinine) in the blood

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7
Q

What is urea?

A

Urea is produced in the liver from ammonia which is a byproduct of protein breakdown in the gastrointestinal tract. Urea is then transported to the kidneys and excreted renally

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8
Q

Which factors can assess serum urea levels?

A

Age
Dietary protein content
Liver dysfunction
Gastrointestinal haemorrhage
Decreased renal excretion
Disruption of urine flow

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9
Q

How can age affect serum urea levels?

A

Young animals tend to have a higher serum urea levels due to the increased endogenous protein catabolism which occurs due to growth

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10
Q

What is creatinine?

A

Creatinine is a byproduct of muscle breakdown and is transported to the kidneys and excreted renally

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11
Q

Which factors affect serum creatinine levels?

A

Reduced muscle mass
Decreased renal excretion
Disruption of urine flow

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12
Q

How does reduced muscle mass affect serum creatinine levels?

A

Creatinine is a byproduct of muscle breakdown and thus serum creatinine levels will be decreased with reduced muscle mass

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13
Q

What determines the rate of renal excretion of urea and creatinine?

A

Glomerular filtration rate (GFR). Thus, if the glomerular filtration rate (GFR) is decreased, this will reduce renal excretion of the urea and creatinine resulting in azotaemia

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14
Q

What are the generalised causes of a decreased glomerular filtration rate (GFR)?

A

Decreased renal perfusion
Decreased renal function
Disruption of urine flow

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15
Q

What are the limitations of serum urea as a marker of decreased glomerular filtration rate (GFR)?

A

Serum urea levels are affected by variable other factors, not just GFR, and urea is not produced at a constrant rate. Furthermore, urea can be reabsorbed into the renal tubules and collecting duct at a variable rate

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16
Q

Why is creatinine a better marker of a decreased glomerular filtration rate (GFR) than urea?

A

Creatinine is a better marker for a decreased glomerular filtration rate (GFR) than urea as it is produced as a constant rate and it is not reabsorbed into the renal tubules or collecting duct

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17
Q

What are the limitations of creatinine as a marker of a decreased glomerular filtration rate (GFR)?

A
  1. Insensitive test as creatinine levels do not increase into the GFR has decreased to 25%
  2. The relationship between serum creatinine levels and GFR is not linear, which means that small changes in creatinine levels within the reference range can mean large declines in GFR
  3. Serum creatinine levels do not tell you why the GFR has decreased
  4. Serum creatinine levels do not discriminate between between acute or chronic kidneys disease
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18
Q

Which other marker can be used to assess for decreased glomerular filtration rate (GFR)?

A

Symmetric dimethylarginine (SDMA) which is a byproduct of protein degradation and is excreted renally

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19
Q

What are the advantages of SDMA as a marker of decreased glomerular filtration rate (GFR) over urea and creatinine?

A

Serum SDMA is not decreased by decreased muscle mass like creatinine
Serum SDMA is a more sensitive test (detects decrease GFR earlier than urea and creatinine)

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20
Q

What should you be remember when you detect azotaemia on biochemistry?

A

If you detect azotaemis on biochemistry, remember that azotaemia does not always equate to kidney disease, and kidney disease does not always result in azotaemia

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21
Q

What is uraemia?

A

Uraemia is a compilation of clinical signs as a result of azotaemia

Be aware that while all uraemic patients are azotaemic, not all azotaemic patients are uraemic

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22
Q

What are the potential clinical signs of uraemia?

A

Inappetence
Depression
Vomiting
Nausea
Diarrhoea
Halitosis
Uraemic oral ulceration/stomatitis

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23
Q

What are the three classifications of azotaemia?

A

Pre-renal azotaemia
Renal azotaemia
Post-renal azotaemia

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24
Q

What is pre-renal azotaemia?

A

Pre-renal azotaemia is azotemia as a result of decreased renal perfusion

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25
Q

What are some of the potential causes of pre-renal azotaemia?

A

Hypovolaemia
Hypotension
Shock
Decreased cardiac output
Aortic/renal thromboembolisms

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26
Q

What is renal azotaemia?

A

Renal azotaemia is azotaemia as a result of intrinsic renal failure

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27
Q

What is post-renal azotaemia?

A

Post-renal azotaemia is azotaemia as a result of a disruption of urine outflow

28
Q

What are some of the potential causes of post-renal azotaemia?

A

Ureterolith
Urethrolith
Lower urinary tract rupture

29
Q

How do you approach determining the cause of azotaemia?

A

History and clinical examination to rule out post-renal azotaemia
Urinalysis to differentiate between pre-renal and renal azotaemia

30
Q

What are some key indicators of pre-renal azotaemia on the history and clinical examination?

A

Decreased fluid intake and/or increased fluid losses can be indicative of pre-renal azotaemia with evidence of dehydration and hypovolaemia on clinical examination

31
Q

What are some key indicators of post-renal azotaemia on the history?

A

Dysuria or stanguria can indicate post-renal azotaemia. (Be aware than anuria and oligouria can be indicative of both post-renal and renal azotaemia). A grossly enlarged bladder on palpation, localised subcutaenous fluid around the perineum or ventral abdomen and/or difficultly or inability to pass a urinary catheter can indicate a post-renal azotaemia

32
Q

How can urinalysis be used to differentiate between a pre-renal and renal azotaemia?

Remember to take your urine sample before beginning fluid therapy

A
  1. If the urine is concentrated, this indicates pre-renal azotaemia (the kidneys have the ability to concentrate the urine) whereas dilute urine indicates renal azotaemia (kidneys are not functioning well enough to concentrate the urine)
  2. Urine sedimentation, tubular casts and haematuria can indicate renal azotaemia (haematuria can also indicate post-renal azotaemia but combine this info with your clinicla exam)
33
Q

What are the urine specfic gravity (USG) values for hyposthenuria?

A

1.000 - 1.007

34
Q

What are the urine specfic gravity (USG) values for isosthenuria?

A

1.008 - 1.012

35
Q

What are the urine specfic gravity (USG) values for hypersthenuria?

A

1.013 - 1.030 (minimally concentrated)
1.030 - 1.050 (well concentrated)

36
Q

What are the key signs of an acute renal azotaemia on history?

A

Acute onset clinical signs
May be a recent history of toxin or drug exposure or anaesthesia
No history of weight loss

37
Q

What are the key signs of an acute renal azotaemia on clinical examination?

A

Kidneys normal to large, maybe painful, on palpation
Usually no signs of anaemia
Good coat condition
Normal body condition score (BCS)

38
Q

What are the key signs of an acute renal azotaemia on clinical pathology?

A

Usually no anaemia
Urine sediment often contains sediment, tubular casts, maybe haematuria
Hyperkalaemia
Metabolic acidosis

39
Q

What are the key signs of chronic renal azotaemia on history?

A

Chronic history of clinical signs
History of weight loss

40
Q

What are the key signs of chronic renal azotaemia on clinical examination?

A

Kidneys usually small and non-painful on palpation
Usually clinical signs of anaemia
Poor coat condition
Poor body condition score (BCS)

41
Q

What are the key signs of chronic renal azotaemia on clinical pathology?

A

Non-regenerative anaemia
Usually no urine sedimentation
Rarely hyperkalaemia
Mild or absent metabolic acidosis

42
Q

What is acute kidney injury (AKI)?

A

Acute kidney injury (AKI) is a sudden, often reversible reduction of elimination and metabolic functions of the kidneys

43
Q

What is acute kidney injury (AKI) classified as if it causes azotaemia?

A

Acute renal failure

44
Q

What are the potential causes of acute kidney injury (AKI)?

A

Decreased renal perfusion
Nephrotoxic drugs
Infectious agents
Toxins
Acute ureteral obstruction

45
Q

Give some examples of nephrotoxic drugs which can cause acute kidney injury (AKI)

A

NSAIDs
Aminoglycosides
Doxorubicin (in cats)
Cisplatin

46
Q

Give some examples of infectious agents which can cause acute kidney injury (AKI)

A

Leptospirosis
Borreliosis (Lyme disease)

47
Q

Give some examples of toxins which can cause acute kidney injury (AKI)

A

Lillies (in cats)
Raisins/grapes (in dogs)
Ethylene glycol

48
Q

What are the four stages of the pathophysiology of acute kidney injury (AKI)?

A

Initiation phase
Extension phase
Maintenance phase
Recovery phase

49
Q

Describe the pathophysiology or acute kidney injury (AKI)

A

During the initiation phase of AKI, something causes damage to the nephrons resulting in renal dysfunction. During the extension phase, there is inflammation, hypoxia and ischaemia which results in further cellular and nephron damage. This is the phase in which clinical and laboratory signs begin to arise. During the maintenance phase, there is ongoing cell death however cellular repair is intiated. During the repair phase, any reversible renal lesions are repaired and remaining nephrons will hypertrophy to compensate

50
Q

How do you approach the diagnosis of acute kidney injury (AKI)?

A

History and clinical signs
Clinical examination
Haematology and biochemistry
Urinalysis
Diagnostic imaging

51
Q

What are the typical clinicopathological findings of acute kidney injury (AKI)?

A

Azotaemia
Hyperkalaemia
Hyperphosphataemia
Hypercalcaemia, normal calcium or hypocalaemia
Increased PCV and TP (dehydration)
Low USG
Urine sedimentation

52
Q

What should you be aware of when an acute kidney injury (AKI) patient has marked hypercalcaemia?

A

You should be aware that hypercalaemia can cause AKI, however AKI can also cause hypercalcaemia

53
Q

Which disease can present very similarly to acute kidney injury (AKI)?

A

Hypoadrenocorticism (Addison’s disease) also presents with azotaemia, hyperkalaemia and a low USG

54
Q

(T/F) Acute kidney injury (AKI) requires emergency treatment

A

TRUE. Acute kidney injury (AKI) requires emergency, supportive treatment

55
Q

Which treatment option should you broach with clients when their pet has acute kidney injury (AKI)?

A

Euthanasia would be an appropirate treatment option to broach with owners in these cases. Treatment for AKI will not speed up the recovery process, it is only supportive treatment which will require hospitalisation, is very expensive and often requires referral

56
Q

What are the general principles for the supportive treatment of acute kidney injury (AKI)?

A
  1. Remove intiating cause of AKI if possible
  2. Restore renal perfusion
  3. Monitor urine output
  4. Monitor electrolytes, acid base balance and hydration status
  5. Treat complications of uraemia
  6. Nutritional support
  7. Investigate the underlying cause of AKI
57
Q

What can you do to monitor urine output?

A

Place an indwelling urinary catheter attached to a urinary bag to monitor urine output

58
Q

What is the normal rate of urine output?

A

1 - 2ml/kg/hr

59
Q

What is anuria?

A

Anuria is when there is no urine output

60
Q

What is oliguria?

A

Oliguria is when there is less than 0.25ml/kg/hr of urine output

61
Q

What is polyuria?

A

Polyuria is when there is more than 2ml/kg/hr of urine output

62
Q

What are the aims of fluid therapy when managing acute kidney injury (AKI)?

A

Restore fluid deficit
Correct electrolyte imbalances
Correct acid base imbalances
Increase urinary output

63
Q

How quickly should you aim to restore the fluid deficit in patients with acute kidney injury (AKI)?

A

You should aim to restore the fluid deficit in patients with acute kidney injury (AKI) within 4 to 6 hours

64
Q

What should you monitor closely for when carrying out fluid therapy in patients with acute kidney injury (AKI)?

A

When carrying out fluid therapy in patients with acute kidney injury (AKI) you should monitor for any signs of fluid overload as the kidneys will be unable to correct it and this can be fatal

65
Q

What can you do to increase urine output in patients with acute kidney injury?

A

If the patient has no signs of fluid overload you could give then an IV fluid bolus of 3-5% of their body weight and monitor them closely for signs of fluid overload. You could also consider diuretics if the fluid deficit has been corrected

66
Q

Which options should you consider if an AKI patient is not improving in response to treatment?

A

Euthanasia
Referral for haemodialysis

67
Q

What is the prognosis for acute kidney injury (AKI)?

A

Poor prognosis (survival of around 50%)

MODULE 17 - Urinary, Endocrine and Oncological Disease (12 decks)

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