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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

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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
Anorexia
Weight loss
Lethargy
Vomiting
Diarrhoea
Ascites
Subcutaneous oedema
Abdominal pain
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 nitrogenous 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 influence 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 constant 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 until 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 kidney 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
What are some of the potential causes of pre-renal azotaemia?
Hypovolaemia Hypotension Shock Decreased cardiac output Aortic/renal thromboembolisms
26
What is renal azotaemia?
Renal azotaemia is azotaemia as a result of intrinsic renal failure
27
What is post-renal azotaemia?
Post-renal azotaemia is azotaemia as a result of a disruption of urine outflow
28
What are some of the potential causes of post-renal azotaemia?
Urolithiasis Lower urinary tract rupture
29
How do you approach determining the cause of azotaemia?
History and clinical examination to rule out post-renal azotaemia Urinalysis to differentiate between pre-renal and renal azotaemia
30
What are some key indicators of pre-renal azotaemia on the history and clinical examination?
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
What are some key indicators of post-renal azotaemia on the history?
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
How can urinalysis be used to differentiate between a pre-renal and renal azotaemia? | Remember to take your urine sample **before** beginning fluid therapy
1. If the urine is concentrated, this indicates pre-renal azotaemia *(the kidneys have the ability to concentrate the urine)* whereas isosthenuric 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 clinical exam)*
33
What are the urine specfic gravity (USG) values for hyposthenuria?
1.000 - 1.007
34
What are the urine specfic gravity (USG) values for isosthenuria?
1.008 - 1.012
35
What are the urine specfic gravity (USG) values for hypersthenuria?
1.013 - 1.030 *(minimally concentrated)* 1.030 - 1.050 *(well concentrated)*
36
What are the key signs of an acute renal azotaemia on history?
Acute onset clinical signs May be a recent history of toxin or drug exposure or anaesthesia No history of weight loss
37
What are the key signs of an acute renal azotaemia on clinical examination?
Kidneys normal to large, maybe painful, on palpation Usually no signs of anaemia Good coat condition Normal body condition score (BCS)
38
What are the key signs of an acute renal azotaemia on clinical pathology?
Usually no anaemia Urine sediment often contains sediment, tubular casts, maybe haematuria Hyperkalaemia Metabolic acidosis
39
What are the key signs of chronic renal azotaemia on history?
Chronic history of clinical signs History of weight loss
40
What are the key signs of chronic renal azotaemia on clinical examination?
Kidneys usually small and non-painful on palpation Usually clinical signs of anaemia Poor coat condition Poor body condition score (BCS)
41
What are the key signs of chronic renal azotaemia on clinical pathology?
Non-regenerative anaemia Usually no urine sedimentation Rarely hyperkalaemia Mild or absent metabolic acidosis
42
What is acute kidney injury (AKI)?
Acute kidney injury (AKI) is a sudden, often reversible reduction of elimination and metabolic functions of the kidneys
43
What is acute kidney injury (AKI) classified as if it causes azotaemia?
Acute renal failure
44
What are the potential causes of acute kidney injury (AKI)?
Decreased renal perfusion Nephrotoxic drugs Infectious agents Toxins Acute ureteral obstruction
45
Give some examples of nephrotoxic drugs which can cause acute kidney injury (AKI)
NSAIDs Aminoglycosides Doxorubicin *(in cats)* Cisplatin
46
Give some examples of infectious agents which can cause acute kidney injury (AKI)
Leptospirosis Borreliosis *(Lyme disease)*
47
Give some examples of toxins which can cause acute kidney injury (AKI)
Lillies *(in cats)* Raisins/grapes *(in dogs)* Ethylene glycol
48
What are the four stages of the pathophysiology of acute kidney injury (AKI)?
Initiation phase Extension phase Maintenance phase Recovery phase
49
Describe the pathophysiology of acute kidney injury (AKI)
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
How do you approach the diagnosis of acute kidney injury (AKI)?
History and clinical signs Clinical examination Haematology and biochemistry Urinalysis Diagnostic imaging
51
What are the typical clinicopathological findings of acute kidney injury (AKI)?
Azotaemia Hyperkalaemia Hyperphosphataemia Hypercalcaemia, normal calcium or hypocalaemia Increased PCV and TP *(dehydration)* Low USG Urine sedimentation
52
What should you be aware of when an acute kidney injury (AKI) patient has marked hypercalcaemia?
You should be aware that hypercalaemia can cause AKI, however AKI can also cause hypercalcaemia
53
Which disease can present very similarly to acute kidney injury (AKI)?
Hypoadrenocorticism (Addison's disease) also presents with azotaemia, hyperkalaemia and a low USG
54
(T/F) Acute kidney injury (AKI) requires emergency treatment
TRUE. Acute kidney injury (AKI) requires emergency, supportive treatment
55
Which treatment option should you broach with clients when their pet has acute kidney injury (AKI)?
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
What are the general principles for the supportive treatment of acute kidney injury (AKI)?
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
What can you do to monitor urine output?
Place an indwelling urinary catheter attached to a urinary bag to monitor urine output
58
What is the normal rate of urine output?
1 - 2ml/kg/hr
59
What is anuria?
Anuria is when there is no urine output
60
What is oliguria?
Oliguria is when there is less than 0.25ml/kg/hr of urine output
61
What is polyuria?
Polyuria is when there is more than 2ml/kg/hr of urine output
62
What are the aims of fluid therapy when managing acute kidney injury (AKI)?
Restore fluid deficit Correct electrolyte imbalances Correct acid base imbalances Increase urinary output
63
How quickly should you aim to restore the fluid deficit in patients with acute kidney injury (AKI)?
You should aim to restore the fluid deficit in patients with acute kidney injury (AKI) within 4 to 6 hours
64
What should you monitor closely for when carrying out fluid therapy in patients with acute kidney injury (AKI)?
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
What can you do to increase urine output in patients with acute kidney injury?
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
Which options should you consider if an AKI patient is not improving in response to treatment?
Euthanasia Referral for haemodialysis
67
What is the prognosis for acute kidney injury (AKI)?
Poor prognosis *(survival of around 50%)*

MODULE 17 - Urinary, Endocrine and Oncological Disease (31 decks)

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