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Renal > Laboratory diagnosis of urinary disease > Flashcards

Laboratory diagnosis of urinary disease Flashcards

1
Q

Define uremia

A

complex of CS and biochemical abnormalities (azotaemia) associated with loss of functional nephrons (i.e. azotemia + CS)

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2
Q

CS - uremia

A
  • anorexia
  • V/D
  • GI haemorrhage
  • ulcerative stomatitis
  • bruxism (ruminants)
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3
Q

Define renal disease

A

presence of morphological or biochemical abnormalities of any size/ severity

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4
Q

Define renal failure

A

biochemical abnormalities present and caused by reduced renal function, coupled with inadequate concentrating ability. Decrease in renal function is teh result of decrease in numbers of functions nephrons (vs decreased function in individual nephrons)

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5
Q

Clinical pathology - renal disease

A 
BEFORE TX!
biochem
UA
haematology
cytology
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6
Q

What is important on routine biochem?

A
  • UN
  • creatinine
  • phosphorous
  • calciium
  • sodium
  • chloride
  • potassium
  • acid base
  • protein
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7
Q

T/F: you need to look at serum/plasma chemistry and urine concurrently

A

True

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8
Q

What are indicators of GFR?

A

urea and creatinine levels (increases assess presence of renal dz/functional impairment)

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9
Q

Where is urea derived from?

A

produced in liver via urea cycle and excreted by kidney - levels influenced by liver function and protein levels

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10
Q

Where is creatinine derived from?

A

from creatine in muscle - levels influence by mm mass

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11
Q

What is UN synthesised from?

A

from ammonia (waste from protein catabolism) via urea cycle in liver

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12
Q

What are urea levels influenced by?

A
  • protein intake

- GIT bleeding

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13
Q

Is UN excreted in faeces?

A

No

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14
Q

How long does it take for UN to equilibrate in vasculature?

A

90 minutes

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15
Q

Cattle can have severe renal dz with relatively normal UN

A

True

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16
Q

What is a reliable indicator of renal dz in ruminants?

A

Creatinine - not urea

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17
Q

Where is urea excreted in ruminants?

A

into rumen and converted to ammonia then aa –> protein synthesis

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18
Q

T/F: if a ruminant is anorectic all urea will be exreted via the GIT and not the kidneys so anorectic ruminants with renal faulure may have va normal UN

A

True

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19
Q

Describe urea and the kidney

A
  • passively filtered by glomerulus (concentration in filtrate same as blood)
  • increased UN largely d/t decreased filtration rate
  • passively diffuses with water from lumen to blood
  • urea absorbed varies inversely with rate of urine flow
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20
Q

T/F: cattle can have severe renal dz with relatively normal UN

A

True

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21
Q

Origin - creatinine

A

from non-enzymatic conversion of creatine (energy stores in mm)

  • constant rate of conversion of creatine to creatinine
  • influenced by mm mass (increases with training) and dz
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22
Q

Describe creatinine distribution through body

A

distributed through ttal body water but diffuses more slowly than urea
- equilibration takes 4 hours (vs 1.5 hours for urea)

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23
Q

Findings suggestive of ruptured bladder (clinical pathology)

A
  • abdominal fluid concentrations of creatinine higher than serum levels
  • difference with serum levels lasts longer than urea
  • comparison of serum and abdominal fluid levels more reliable than urea
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24
Q

What is creatinine affected by?

A

not by diet or catabolic factors

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25
Q

What is the sensitivity of creatinine for diagnosing renal dz?

A

poorly sensitive - 3/4 renal function must be lost (dogs)

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26
Q

In which spp is creatinine a more sensitive indicator of renal dz?

A

cow and horse

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27
Q

Why is creatinine a v insensitive diagnostic test in birds?

A

-

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28
Q

Outline birds and nitrogen catabolism

29
Q

What are the types of azotaemia?

A
  • PRERENAL: d/t reduced renal perfusion or increased protein catabolism. Prerenal leads to renal azotaemia eventually.
  • RENAL: d/t renal disease and presence of nonfunctional nephrons
  • POSTRENAL: d/t interference with the excretion of urine (obstruction or postrenal leakage)
30
Q

Causes - pre-renal azotaemia

A
  • ** reduced renal concentration as with haemoconcentration
  • increased protein catabolism secondary to gastric or small bowel haemorrhage, necrosis, starvation, corticosteroids
  • high protein diets
31
Q

T/F: diseases causing pre- or post renal azotemia may secondarily affect the kidneys and lead to renal azotemia

32
Q

Why is USG high in pre-renal azotemia?

A

because ADH response occurs and kidneys concentrate urine

33
Q

When does renal azotemia occur?

A

when 3/4 nephrons are non-functional (dogs)

34
Q

What causes azotemia in renal azotemia?

A

insufficient excretion of UN and creatinine

35
Q

CS - post-renal azotemia

A
  • oliguira or anuria
  • USG may vary
  • UN and creatinine should return to normal once obstruction relieved or source of leakage is repaired
36
Q

What should you compare USG with?

A

serrum/plasma urea and creatinine

37
Q

Define USG

A

ratio of refractive index of water compared to water. Depends on particle size, weight and number. Determined by refractomer. Good reflection of osmolality.

38
Q

How may USG be falsely increased?

A

glucose or protein in urine

39
Q

USG range - healthy animals

A

1.001 - 1.065 (up to 1.080 in cats)

40
Q

What should USG be if urea and creatinine are increased in serum/plasma?

A

1.030 in a dog
1.035 in a cat
1.025 in horses/ruminants
(if USG is less than these values, there is decreased concentrating ability and renal failure is present)

41
Q

Define isosthenuria

A
  • fixed USG 1.008 - 1.012

- kidney not concentrating or diluting urine so osmolality is same as glomerular filtrate

42
Q

Define hyposthenuria

43
Q

What components of the biochem panel can be used to assess renal function?

A
  • electrolytes (Na, K and Cl)
  • phosphorous
  • calcium
  • protein/albumin
  • amylase and lipase
44
Q

Main ion in ECF

45
Q

Regulation - Na

A
  • levels regulated by kidney (like water)
  • 75% reabsorbed in PCT
  • aldosterone stimulates Na reabsorption in CD
46
Q

Causes increased Na

A
  • increased intake
  • increased water loss
  • decreased water intake
47
Q

Causes - decreased Na

A
  • increased loss *

- increased water intake

48
Q

What do chloride changes usually coincide with?

A

changes in sodium. changes without changes in Na are often associated with changes in acid/base status.. Interference from bromide and iodine salts

49
Q

Define azotaemia

A

an increase in the non-protein nitrogenous compounds, usually urea nitrogen (UN) and/or creatinine or uric acids (birds) in the blood

50
Q

Main ion in intracellular space = ?

51
Q

Regulation - K

A

by intake and secretion in CDs under aldosteroe

52
Q

Causes - Increased K+

A
  • renal failure (especially if anuria or oliguria present)
53
Q

Causes - decreased K+

A
  • loss (renal, V, D)
  • decreased intake
  • hypoadrenocorticism
  • cell leakage (tissue damage, thrombocytosis/leukaemia)
54
Q

How is K+ affected in acidosis?

A

K+ increases relative to its level before the acidosis

55
Q

Is assessing acid base status from serum biochem reliable?

56
Q

How is it best to asses acid base status?

A

blood gases

57
Q

How is calcium measured?

A
  • free calcium - active (50% total)
  • bound calcium - to albumin (40-45%)
  • bound calcium - to non-protein anions (5-10%)
  • total calcium affected by albumin levels - of albumin is decreased so will Ca)
58
Q

What should you do if you detect increased Ca?

A

check free Ca levels separately to confirm

59
Q

What happens to Ca in renal failure?

A

increased amount is bound to anions (PO4, citrates, sulphates)

60
Q

What are Ca levels regulated by?

A
  • PTH
  • vitamin D
  • calcitonin
61
Q

What are the Ca levels of most dogs /cats with renal failure? Cattle? Horses?

A
  • hypo or normocalcemic
  • cattle will be hypocalcemic
  • horses will be hypercalcemic as kidney is major excretory route for calcium
62
Q

What is hyperphosphataemia associated with?

A

decreased GFR so levels increased in dogs/cats with renal dz

63
Q

Whya re horses with renal dz hypophosphataemic?

A

Mechanism unknown

64
Q

Describe phsophorous levels in young growing animals?

A
  • increased phosphorous

- elevated Ca and ALP too

65
Q

Why does secondary renal hyperparathyroidism occur?

A
  • d/t renal dz –> reduced 1a-hydroxylase –> decreased 1,25 DHCC –> increased PTH
  • decreased fCa2+ absorption from GIT and resorption from bone –> decreased fCa2+ –> increased PTH
66
Q

How might primary glomerular disease affect protein levels?

A
  • -> severe hypoproteinemia d/t hypoalbuminaemia (preferentially lost)
  • possible concurrent hyperlipidema and hypercholesterolemia
  • proteinuria and v high protein: creatinine
67
Q

Are amylase and lipase affected by kidney disease?

A
  • cleared by kidney so modest increases can be seen in dogs with renal dz
  • TLI also increased by reduced GFR
68
Q

Characterise the anaemia of renal dz

A
  • mild (in dogs, HCT shouldn’t be
69
Q

When is urine cytology useful?

A
  • dx of renal lymphoma (if both kidneys enlarged)
  • bladder neoplasia: do histopathology or urine cytology, not sediment exam
  • biopsy for all other dz as can assess architecture *

Renal (30 decks)

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