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Thrall > Renal > Flashcards

Renal Flashcards

1
Q

4 things GFR depends on:

A

1) adequate blood flow, 2) BP, 3) interstitial and intratubular pressures, 4) number of functioning nephrons

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2
Q

GFR has to be decreased by ____% before BUN and Cr increase.

A

75%

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3
Q

Urine concentrating ability is lost after ___% of nephrons are gone.

A

66%

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4
Q

After creatinine is increased, every doubling of Cr means there’s been loss of function of ___% of the remaining renal mass.

A

50%

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5
Q

What are some tests used to measure GFR?

A

endogenous/exogenous Cr clearance
insulin clearance
clearance of radioisotopes
measurement of fractional clearance of electrolytes

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6
Q

What is the formula for Cr clearance?

A

Cr clearance= [(Urine Cr x vol urine/time/kg)/ serum Cr]

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7
Q

What are 4 reasons that Cr is better than BUN for determining GFR.

A

1) rate of production and exertion of Cr is constant, 2) Cr isn’t metabolized by external or renal processes, 3) some BUN in the filtrate is reabsorbed, 4) rate of BUN resorption varies w/hydration status and speed of flow in tubules

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8
Q

Between BUN and Cr, which can be disproportionately higher in dehydration? Why?

A

BUN (rate of BUN resorption varies w/hydration status and speed of flow in tubules)

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9
Q

What does an increased BUN:Cr ratio indicate? (2)

A

dehydration of intestinal bleeding

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10
Q

What does a decreased BUN:Cr ratio indicate? (3)

A

diuresis, noncreatinine chromagens, or ability of cows/horses to excrete BUN from GI

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11
Q

What are the 5 locations that can have lesions leading to renal azotemia?

A

glomeruli, tubules, interstitium, renal pelvis, blood vessels

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12
Q

Creatinine: Made in the ____ from the spontaneous conversion of ____ and ____.

A

Made in the muscles from the spontaneous conversion of creatine and creatine phosphate.

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13
Q

What is a major mechanism of non-renal increases in Cr?

A

muscle catabolism

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14
Q

What are 3 scenarios where you could have incr Cr from incr muscle catabolism.

A

Sepsis, developing cachexia, rhabdomyolysis

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15
Q

What is are 3 scenarios where you could have dear Cr?

A

liver failure (rare), cachexia, hyperthyroidism

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16
Q

What should you think about in cattle and horses if the Cr is significantly increased and the BUN is normal or a little high?

A

Non-creatinine chromagens

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17
Q

What are 4 important non-creatinine chromogens?

A

ketones, glucose, carotenes, Vit A

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18
Q

Interpret the scenario in a cow/horse:

USG & Cr incr, BUN normal

A

non-Cr chromagens causing Cr increase

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19
Q

Interpret the scenario in a cow/horse:

USG & BUN incr but Cr disproportionately higher than BUN

A

prerenal azotemia & non-Cr chromagens causing incr

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20
Q

Interpret the scenario in a cow/horse:

Isosthenuria w/azotemia but Cr disproportionately higher than BUN

A

renal azotemia but the discrepancy could be b/c of non-Cr chromogens or the fact that they can excrete BUN in GI

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21
Q

Between BUN and Cr, which will be present in the abdominal fluid of an animal with ruptured bladder longer and why?

A

Cr b/c it takes longer for Cr to equilibrate with serum than BUN

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22
Q

Dialysis and diuresis promote greater excretion of ___ than ____ (BUN or Cr)

A

Dialysis and diuresis promote greater excretion of BUN than Cr.

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23
Q

___% of BUN is passively resorbed by the proximal tubules, ___% by the collecting ducts.

A

50% of BUN is passively resorbed by the proximal tubules, 10% by the collecting ducts.

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24
Q

What happens to the urea secreted in saliva of small animals?

A

goes to GI–> degraded to ammonia by back–> reabsorbed–> to liver–> turned back into urea

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25
Q

What happens to urea secreted in saliva of ruminants (and some degree in horses)?

A

goes to rumen–> bacteria turn urea into amino acids–> aas from the breakdown reabsorbed so get net protein gain and net urea loss

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26
Q

Why does rumen stasis cause increased BUN without Cr?

A

Because the urea secreted in saliva goes to rumen but not broken down and reabsorbed as aas

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27
Q

How does GI bleeding cause an increase in BUN?

A

blood is broken down into aas and ammonia in the GIT–> reabsorbed and go to liver where they’re converted back to urea

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28
Q

4 nonrenal causes of increased BUN

A

1) high pr diet, 2) GI hemm, 3) sepsis/fasting (incr protein catabolism), 4) decr renal perfusion (increases renal tubular resorption)

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29
Q

6 causes of decreased BUN

A

1) liver failure, 2) shunts, 3) malnutrition or low pr diet, 4) hyperthyroidism (incr pr catabolism and incr GFR), 5) diuresis, 6) young animals (high anabolic state)

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30
Q

2 major mechanisms of prerenal azotemia

A

1) increased pr catabolism (small bowel hemm, necrosis, starvation, prolonged exercise, infection, fever, steroids); 2) hypovolemia (dehydration, cardiac insufficiency, shock)

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31
Q

5 nonrenal conditions where you have dehydration but can’t concentrate urine

A 
primary and secondary DM
hyperCa
steroids
pyometra
medullary washout
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32
Q

What is the expected urine Cr:serum Cr ratio to distinguish renal from prerenal azotemia?

A

> 50:1 prerenal

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33
Q

Normal fractional excretion of Na is

A
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34
Q

T or F: With primary glomerular disease, you always get decreased concentrating ability before azotemia.

A

False: With primary glomerular disease, you may get azotemia before a decrease in concentrating ability because tubular disease usually follows glomerular.

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35
Q

Why might horses only get a moderate increase in BUN with renal failure?

A

Because they can excrete it in their GI– so if BUN is really high, likely has prerenal component

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36
Q

Why isn’t BUN a good indicator of renal disease in birds? What is a better indicator?

A

they don’t have a lot of urea in the blood to begin with. Uric acid is better

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37
Q

What is the main end-product of nitrogen catabolism in birds?

A

uric acid

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38
Q

What are 2 non-renal causes of hyperuricemia in birds?

A

ovulation and post-meal

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39
Q

The kidneys resorb ___% of H2O that enters the tubules.

A

99%

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40
Q

Water is resorbed passively in everywhere in the kidneys except the _____ where ____ acts.

A

Water is resorbed passively in everywhere in the kidneys except the collecting tubules where ADH acts.

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41
Q

What are 5 factors needed to make concentrated urine?

A

1) 1/3 renal mass functioning, 2) enough ADH made and able to respond to it, 3) medullary interstitium saturated, 4) conducive hydration status, 5) no concurrent diseases

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42
Q

T or F: Birds have a bladder.

A

False

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43
Q

6 mechanisms that can lead to decreased urine concentrating ability.

A
  1. lesions in 2/3 of the kidney
  2. decreased ADH production (CDI)
  3. refractory to ADH
  4. decreased medullary hypertonicity (washout)
  5. overhydration
  6. solute overload (DM, diuresis)
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44
Q

The water deprivation test is used to differentiate between which 3 diseases/conditions?

A

PD
CDI
RF (before azotemia)

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45
Q

A major contraindication to doing the water deprivation test is what?

A

azotemia

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46
Q

What is the mechanism of the water deprivation test?

A

Induces

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47
Q

What is the maximum weight loss stimulus for ADH release?

A

3-5%

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48
Q

What are 2 scenerios that using the water deprivation test would be indicated?

A

1) PUPD in an animal without azotemia, dehydration, or other biochemical abnormalities
2) repeated urine samples in nonazotemic patients with isosthenuria

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49
Q

When should you stop the water deprivation study (multiple)?

A

When they are concentrating to 1.025-1.035 or
5% of BW lost or
azotemia develops

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50
Q

When should you give ADH during a water deprivation study?

A

if the USG changes 310 most/kg or 3-5% weight loss

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51
Q

Water deprivation study: if the patient has PD, how fast should the urine start to become concentrated?

A

within a few hours

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52
Q

Water deprivation study: If the urine is not concentrating after a few hours, what are the differentials and what is ruled out?

A

Differentials are DI or renal failure

PD is ruled out

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53
Q

Water deprivation study: If a patient cannot concentrate their urine after a few hours but starts to concentrate after ASH is given, what is the dx?

A

CDI

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54
Q

Water deprivation study: If a patient cannot concentrate its urine after a few hours and ADH is given, but there is still no response, what are the differentials?

A

Renal failure or NDI but bloodwork should help differentiate between those

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55
Q

What is another test you can do to test concentrating ability if the water deprivation test is too risky (but is less sensitive than the WDT)?

A

ADH concentration test

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56
Q

Main differentials for persistent isosthenuria without azotemia?

A

CDI or NDI

PD

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57
Q

Urine specific gravity is an estimate of ______.

A

Urine specific gravity is an estimate of osmolality.

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58
Q

The urine filtrate starts with a USG of ____ and osmolality of _____.

A

The urine filtrate starts with a USG of 1.010 and osmolality of 300 most/kg.

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59
Q

Main differentials in a patient with persistent hyposthenuria without azotemia?

A

NDI/CDI

PD

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60
Q

USG is an estimate of _________.

A

osmolality

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61
Q

What is the relationship between osmolality and freezing temperature?

A

As osmolality increases, the freezing temp decreases (lower temp required to freeze).

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62
Q

T of F: Mucus, crystals, and cells affect USG.

A

False

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63
Q

For every 1 g/dL of protein and glucose in urine, the USG increases by ____.

A

0.004

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64
Q

T or F: Hetastarch increases osmolality but not USG.

A

True

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65
Q

Urine volume and Spg are inversely correlated in health and most diseases except which 2?

A 
DM (incr vol w/incr Spg)
Oliguric RF (decr vol w/decr Spg)
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66
Q

Isosthenuria in dog, cat, cow, horse.

A

1.007-1.013

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67
Q

Hyposthenuria in dog, cat, cow, horse.

A
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68
Q

Adequate concentrating ability Usg in a dog.

A

> 1.030

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69
Q

Adequate concentrating ability Usg in a cat.

A

> 1.035

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70
Q

Adequate concentrating ability Usg in a horse.

A

> 1.025

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71
Q

Adequate concentrating ability Usg in a cow.

A

> 1.025

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72
Q

5 causes of NDI.

A 
HyperCa
Steroids
HypoK
Pyometra
Congenital
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73
Q

4 causes of solute overload leading to PU/PD and dilute urine.

A

DM
acromegaly
Faconi’s
salt toxicity

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74
Q 
Changes to urine when left at room temp:
Cells and casts-
Glucose-
Ketones and bilirubin-
pH-
CO2-
Bacteria-
A 
Cells and casts- lyse
Glucose-metabolized
Ketones and bilirubin- decrease
pH- increases (urea converted to ammonia)
CO2-escapes
Bacteria- proliferates
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75
Q

Normal urine production per day in a dog.

A

20-40 ml/kg/day (1 ml/kg/hr)

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76
Q

Normal urine production per day in a cat.

A

10-20 ml/kg/day

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77
Q

6 potential causes of red/brown urine.

A 
hemoglobinuria
myoglobinuria
hematuria
porphyria
phenothiazine antihelmnitics
aminopyrine (urinary analgesic)
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78
Q

What is unique about porphyrins in urine?

A

Fluoresce under UV light

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79
Q

Normal urine pH in dog and cat.

A

5-7

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80
Q

Normal urine pH in horse and cow.

A

7-8

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81
Q

Normal WBC or RBC seen in urine of dog, cat, horse, cow.

A

0-5

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82
Q

Proteinuria indicates a lesion in which part of the kidney?

A

Glomerulus

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83
Q

Casts indicate a lesion in which part of the kidneys?

A

Tubules

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84
Q

USG is lower in puppies

A
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85
Q

T or F: there is no difference in protein, blood, ketones, or bilirubin in puppy urine.

A

True

86
Q

With paradoxical aciduria, what has to be corrected before the tubules can excrete bicarb?

A

HypoCl

87
Q

What are the main chem/urine findings in paradoxical aciduria?

A

Profound hypoCl
Increased bicarb
Acidic urine

88
Q

What is a differential to consider in a dog with acidosis but alkaline urine?

A

RTA

89
Q

Struvites form in alkaline/acidic urine?

A

alkaline

90
Q

Differentials in dogs with alkaline urine (4)

A

RTA
Urease splitting bacterial infections
long storage time at room temp
disinfectant contamination

91
Q

How does the protein pad on the dipstick work?

A

it is kept at an acidic pH and when anionic proteins (albumin) hit it, it becomes alkalinized and changes color

92
Q

Trace proteinuria is ____ g/dL.

A

Trace proteinuria is

93
Q

1+ proteinuria is ____ g/dL.

A

1+ proteinuria is 0.03 g/dL.

94
Q

Bence Jones proteins won’t case a + on the dipstick until ____ g/dL.

A

0.025- 0.05 g/dL

95
Q

The SSA turbidity test is a test for what?

A

Proteinuria

96
Q

T or F: The SSA test only picks up albumin.

A

False- it picks up all proteins

97
Q

What can cause a false + on the SSA test?

A

Penicillin, sulfonamides, contrast media

98
Q

What can cause a false - on the SSA test?

A

turbid or markedly alkaline urine

99
Q

What causes a false + on the protein pad (dipstick) but a false - on the SSA test (if marked)?

A

alkalinuria

100
Q

What can cause a false + on the blood pad of the dip stick because of lysis?

A

very dilute urine (

101
Q

What are 2 causes of false +s on the glucose pad on the dipstick?

A

oxidizing cleaning agents or H2O2 touching the pad

cats with urethral obstruction (unknown compound causes it)

102
Q

Renal threshold for glucose in dog.

A

200 mg/dL

103
Q

Renal threshold for glucose in cat.

A

300 mg/dL

104
Q

Renal threshold for glucose in horses.

A

150 mg/dL

105
Q

Renal threshold for glucose in cattle.

A

100 mg/dL

106
Q

Glucosuria without serum glucose over the threshold suggests what?

A

Renal tubular resorption defect or transient hyperglycemia causing glycosuria but blood taken after it has normalized

107
Q

Differentials for glucosuria without serum glucose over threshold (non-transient).

A

nephrosis (toxic)
tubular injury
primary or familial glucosuria
fanconis

108
Q

Ketones are measured on the dipstick via a ____ reaction.

A

Nitroprusside

109
Q

Excreted ketones include ___% beta-hydroxybutyrate, ___% acetoacetic acid, and ___% acetone.

A

78% beta-hydroxybutyrate, 20% acetoacetic acid, and 2% acetone.

110
Q

7 differentials for ketonuria.

A 
excessive fat catabolism (neg energy balance)
low carb diet
cachexia
starvation
hyperthryoidism
preg toxemia
DM
111
Q

What might happen to Na and/or K with ketonuria?

A

It can cause hypoNa and/or hypoK because ketone needs to be excreted with a cation

112
Q

Does biliverdin cause a + reaction on the bilirubin pad on the dipstick?

A

no

113
Q

T or F: The bilirubin pad on the dipstick only detects unconjugated bilirubin.

A

False– only conjugated bilirubin

114
Q

Does bilirubinemia or bilirubinuria come first?

A

bilirubinuria

115
Q

RBC casts localize hemorrhage to the ____.

A

tubules

116
Q

WBC casts localize inflammation to the ___ and indicate ____.

A

WBC casts localize inflammation to the tubules and indicate pyelonephritis.

117
Q

If you see a bunch of squames in a free catch urine from a male dog, what differential should be considered?

A

Sertoli cell neoplasm (secreting estrogen and causing squamous metaplasia of the prostate)

118
Q

5 reasons you may see bacteria in urine with pyuria.

A 
contamination
Cushings 
exogenous steroids
dilute or alkaline urine (lyse WBCs)
antibiotics
119
Q

Lipid is common in the urine of ____.

A

cats– their renal tubular cells have a lot of lipid normally

120
Q

T or F: Lipiduria is correlated with lipemia.

A

F

121
Q

Hyaline casts are made from ___ and ___.

A

mucoprotein and albumin

122
Q

An increase in hyaline casts implies what?

A

glomerular disease or Bence Jones proteinuria

123
Q

Granular casts indicate ___, ___, or ____.

A

Granular casts indicate nephrosis, pyelonephritis, or infarction

124
Q

Waxy casts indicate what?

A

Chronic progressive tubulointerstitial disease

125
Q

___/lpf grabular casts in concentrated urine is normal

A

1-2/lpf

126
Q

Waxy casts form in ____.

A

collecting tubules

127
Q

Lipid seen in pathologic states (so not just in cats that normally have it) can occur with what 2 disease?

A

tubular disease/degeneration and DM

128
Q

Ammonium biurate crystals can normally be seen in what breeds? What is the pathogenesis?

A

dalmations and bulldogs

defect in uric acid transporter into hepatocytes so excrete uric acid in urine

129
Q

What are 2 pathologic states that you can see ammonium biurate crystals in?

A

Liver failure, shunt

130
Q

Bilirubin crystals occur in alkaline/acidic urine?

A

acidic

131
Q

What kinds of animals normally have Ca carbonate crystals?

A

herbivores like horses, rabbits, GPs

132
Q

What kind of crystals are normally common in birds?

A

amorphous urates

133
Q

In what situation may you see a non-pathologic increase in the number of Ca oxalate dehydrate crystals seen in horse and cow urine?

A

when they’re eating oxalate-rich plants

134
Q

What differentials should be considered in dogs or cats with increased numbers of Ca oxalate dehydrate crystals?

A

can be normal
EG toc
hyperCa disorders

135
Q

T or F: Ca oxalate monohydrate crystals can be seen in normal dogs, cats, horses, rabbits, and GPs

A

T

136
Q

Ca phosphate crystals normally form in alkaline/acidic urine?

A

Alkaline

137
Q

Why might you see cholesterol crystals in urine?

A

hypercholesterolemia

PLN

138
Q

What drugs most often cause crystalluria?

A

sulfas, ampicillin, allopurinol, xanthine, contrast media

139
Q

Hippuric acid crystals look like which other crystal?

A

Ca oxalate monohydrate

140
Q

Leucine crystals suggest what?

A

liver disease

141
Q

Tyrosine crystals can be seen with what?

A

liver disease

142
Q

Uric acid crystals have the same pathology as what other crystal?

A

urates (can see in dalmatians or in liver disease)

143
Q

What is the pathologic process that leads to formation of uric acid crystals in liver disease?

A

can’t concert uric acid to allantoin and ammonia to urea

144
Q

xanthine crystals look exactly like what other type of crystal?

A

ammonium biurate

145
Q

Xanthine crystals can be familial in what breeds?

A

doxies and cavies

146
Q

Xanthine crystals can form with administration of what medication?

A

allopurinol

147
Q

Most small animals with renal disease have increased/decreased/normal P and increased/decreased/normal Ca.

A

Most small animals with renal disease have increased P and normal Ca.

148
Q

The second most common changes seen in small animal patients with renal disease in Ca and P are: increased/decreased/normal P and increased/decreased/normal Ca

A

The second most common changes seen in small animal patients with renal disease in Ca and P are: increased P and decreased Ca.

149
Q

What are the 6 mechanisms that lead to hypocalcemia in renal disease (SA)?

A 
not enough tubular cells to resorb it
decr Vit D production
decr albumin 
soft tissue mineralization
secondary to P increase
chelation from oxalate with EG tox
150
Q

Only about __-__% of small animals with renal disease have hyperCa.

A

10-20%

151
Q

HyperCa more commonly occurs in renal disease in small animals with what condition?

A

familial renal nephropathy

152
Q

Horses most commonly have increased/decreased/normal Ca in renal disease. P is 50/50 incr and decr.

A

increased

153
Q

Are cows with RF more likely alkalotic or acidotic?

A

Alkalotic because of ruminal atony & ileum from uremia

154
Q

Ill cows are often hypoCa…why is this?

A

Ill cows often get ruminal atony and ileus which causes alkalosis. Alkalosis causes a shift of iCa to protein bound Ca.

155
Q

___% of P is resorbed in the prox tubule, ___% excreted.

A

80% of P is resorbed in the prox tubule, 20% excreted.

156
Q

A P >___ mg/dL is considered severe.

A

15 mg/dL

157
Q

What are 4 common sites that become mineralized with a high Ca x P?

A

blood vessels, midzonal gastric mucosa, heart, lungs

158
Q

What is the mechanism for developing metabolic bone disease, osteopenia, renal fibrous osteodystrophy from CRF?

A

CRF–> decr Vit D–> can’t resorb Ca or get from bones–> parathyroid hyperplasia–> incr PTH–> Ca resorbed in kidneys and get more from bones

159
Q

How correction of metabolic acidosis cause hypoCa?

A

Ca will go from ionized in acidosis to protein bound in alkalosis.

160
Q

Why aren’t patients with hyperCa of malignancy hyperP?

A

because PTH-rp acts like PTH which is phosphaturic

161
Q

If you have hyperP with a much higher hyperCa with azotemia, is renal failure or a primary Ca disorder (like hyperCa of malign or primary hyperPTHism) more likely?

A

Primary Ca disorder b/c Ca is much higher

162
Q

If you have hyperP with a much higher hyperCa with azotemia, a primary Ca disorder is more likely than renal failure. Between hyperCa of malign and primary hyperparathyroidism, which is more likely in this case?

A

HyperCa of malignancy because only 5% of patients with hyperparathyroidism have azotemia.

163
Q

What do you think is going on if you have a patient with normal P, hyperCa, and azotemia?

A

Think primary Ca disorder (hyperCa of malign or primary hyperPTHism) that’s causing phosphaturia.

164
Q

What are 4 mechanisms that hyperCa causes dilute urine?

A

Interferes w/ADH action
Decreases movement of AQP2 to apical membrane to prevent H2O resorption
Blocks receptors on renal epis
Mineralization of cells

165
Q

Cows and horses are usually hyper/hypo/normo Na and hyper/hypo/normo Cl with renal failure.

A

Cows and horses are usually hypoNa and hypoCl with renal failure.

166
Q

___% of Na is resorbed in the kidney– __% in prox convoluted tubule, __% in the ascending LOH, ___% in each distal tubule and collecting duct.

A

100% of Na is resorbed in the kidney– 65% in prox convoluted tubule, 25% in the ascending LOH, 5% in each distal tubule and collecting duct.

167
Q

What are 2 differentials when the FE of Na is over 1%?

A

RF or decreased aldosterone

168
Q

Most cases of small animal renal failure have hyper/hypo/normo Na and hyper/hypo/normo Cl unless chronic and then there may be hyper/hypo/normo Na and hyper/hypo/normo Cl.

A

Most cases of small animal renal failure have normoNa and normoCl unless chronic and then there may be hypoNa and hypoCl.

169
Q

Cl and Na are expected to be high/low/normal in cases of uroabdomen in all species.

A

low Na and Cl

170
Q

Most K is resorbed in the ____ and excreted in the ___ via _____.

A

Most K is resorbed in the pro tubule and excreted in the CD via aldosterone.

171
Q

HypoK in cats with renal failure put them at risk for what?

A

kaliopenic polymyopathy-nephropathy syndrome

172
Q

SAs with chronic renal failure are more likely to have hyper/hypo/normo K?

A

hypo

173
Q

What are the mechanisms responsible for hypoK in cows with RF?

A

renal loss, salivary loss, anorexia, met alkalosis from ruminal atony causes K to shift into cells

174
Q

How does hypoK make renal failure worse?

A

causes tubular degeneration and decreased responsiveness to ADH

175
Q

Where is most Mg resorbed?

A

prox tubule and thick ascending LOH

176
Q

Mg is usually high/low/normal in patients with RF.

A

high

177
Q

Ca and Mg pattern in blister beetle tox?

A

severe hypoCa and hypoMg

178
Q

P in horses with CRF is usually high/low/normal?

A

low (different than SAs & cows)

179
Q

Formula for determining FE of an electrolyte?

A

FE = [serum Cr/urine Cr] x [urine electrolyte/serum electrolyte] x 100

180
Q

HypoNa azotemic animal with FE of Na

A

GI Na loss

181
Q

What does a FE of P >20 in a dog and >73 in a cat indicate?

A

increased PTH or PTHrp

182
Q

What is the typical pattern of Na, Cl, K, and acidosis vs alkalosis in cows w/RF?

A

hypoNa, hypoCl, hypoK; usually met alk b/c of ruminal atony but can have acidosis from uremia

183
Q

3 conditions that have to occur for paradoxical acuduria to happen.

A

hypoCl, dehydration, met alkalosis

184
Q

What is the mechanism for paradoxical aciduria?

A

dehydration–> RAAS triggered–> aldosterone to kidney–> Na/H2O resorbed but K has to be excreted for this to happen–> at same time aldosterone triggers H excretion which wants to leave with Cl but hypoCl prevents that–> so leads to bicarb formation in tubules which is resorbed in exchange for H

185
Q

Some of the highest fibrinogen concentrations in cows are seen with what condition?

A

RF

186
Q

2 main glomerular diseases?

A

glomerulonephritis and amyloidosis

187
Q

What are some sources/causes of preglomerular proteinuria?

A

overloading– myoglobin, Hg, paraproteins

transient from fever, stress, seizures, and exercise

188
Q

Hypoalb + persistent proteinuria + inactive sediment indicate a lesion in which part of the kidney?

A

glomerular

189
Q

What changes are seen with nephrotic syndrome?

A

hypercholesterolemia, proteinuria, hypoalb

also edema, ascites, thrombi

190
Q

Why might kids, foals, calves, and lambs

A

colostrum ingestion

191
Q

Creatinine is usually measured via the ___ reaction.

A

Jaffe

192
Q

UPUC: >___ indicates renal proteinuria

A

> 1

193
Q

A normal UPUC is

A
194
Q

What is the point of the microalbuminuria test?

A

To detect trace protein that might be present in early renal disease

195
Q

What are 2 ways that glomerular disease can lead to a prothrombotic state?

A
  1. AT lost in urine

2. albumin lost in urine–> increases plt sensitivity

196
Q

Why isn’t hyperP as significant in a cow with dear GFR as other species?

A

Because they secrete P in other locations other than the kidney.

197
Q

Why is PTH important in renal failure?

A

It increases because of decreased GFR which can lead to fibrous osteodystrophy or osteopenia. Also, PTH acts as a uremic toxin.

198
Q

Does Vit D increase or decr in renal failure?

A

Decrease because it can’t be converted to active form in the nonfunctioning kidneys.

199
Q

An increase in the amount of GGT or NAG in the urine in renal disease indicates what?

A

indicates ongoing proximal tubular lesion because this is where most of these enzymes are and are washed out with each urination when released in tubular injury

200
Q

Ormolu gap is defined as-

A

the difference between the measured osmolality and calculated osmolarity

201
Q

What is the formula to calculate osmolality?

A

1.86 ([Na + K] + Glucose/18 + BUN/2.8)

202
Q

What are the osmole gap RIs?
___= normal
___= suggestive of EG tox
___= diagnostic of EG tox

A

What are the osmole gap RIs?
20= suggestive of EG tox
>30= diagnostic of EG tox

203
Q

What is the AG calculation?

A

AG= (Na + K) - (Cl + HCO3)

204
Q

What is the toxic metabolite with diethylene glycol toxicity?

A

HEAA

205
Q

What are the expected serum BUN, Cr, K, P, Na, & Cl in uroabdomens?

A

incr BUN, Cr, K, P

decr Na, Cl

206
Q

What makes up the counter current multiplier system?

A

hypertonic medullary interstitium and the vasa recta

207
Q

Fanconi syndrome is from a defect in what?

A

defect in proximal tubule resorption in glucose, Na, Ca, bicarb, amino acids, and/or P

208
Q

What are some findings in the urine in a patient with Fanconis?

A

dilute urine, glucosuria, proteinuria, increased FE of electrolytes, cystinuria, aminoaciduria

209
Q

Patients with nephrotic syndrome have a lesion at the level of ____.

A

the glomerulus (from amyloidosis, glomerulonephritis, or end stage RF)

210
Q

Puppies/young dogs with progressive renal nephropathy/dysplasia typically have increased/decreased/normal Ca and P.

A

hyperCa and hyperP

211
Q

Why would one consider running a bFGF test on urine?

A

if bladder cancer is suspected

Thrall (4 decks)

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