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RUSVM Clin Path > Renal Disease > Flashcards

Renal Disease Flashcards

1
Q

Azotemia

A

increased urea nitrogen with/without increased creatinine

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2
Q

uremia

A

excessive urea in blood with clinical signs of renal failure

vomiting, diarrhea, ammoniacal breath odor

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3
Q

renal function

A

Produce hormones (EPO, Renin)

Activate vitamin D (Ca, Phos homeostasis)

Regulate blood pressure (RAAS)

Excretes waste products

Conserves important substrates (WATER!)

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4
Q

T/F kidneys have a large functional capacity if basement membrane is intact

A

true

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5
Q

with loss of nephrons:

A

‒ Lose the ability to concentrate urine (1st)

‒ Become azotemic (2nd)

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6
Q

serum chemistry

A

‒ Urea Nitrogen concentration (BUN, UN, SUN)

‒ Creatinine concentration (Crea, Cre, Ct)

‒ Symmetric dimethylarginine (SDMA-new IDEXX test)

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7
Q

Urine tests

A

‒ Urine Specific Gravity (SpGr, USG)

‒ Urine Protein Concentration

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8
Q

Specialized Testing

A

‒ Urine Protein: Creatinine Ratio (UPCR)

‒ Fractional excretion of protein

‒ Fractional excretion of electrolytes

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9
Q

Blood Urea Nitrogen (BUN)

A

Synthesized in the liver

Urea is measured as BUN

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10
Q

the majority of urea is excreted by

A

the kidney

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11
Q

T/F any analyte filtered by the glomerulus is an indicator of GFR

A

true

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12
Q

is BUN an indicator of GFR

A

yes, filtered by glomerulus but there are better ones

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13
Q

BUN concentration varies with the rate of:

A

1.Production by the liver

  1. Reabsorption by the:
    • Kidney (all species)
    • GI tract (ruminants)
  2. Excretion by the kidney
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14
Q

what can cause increased protein in the upper GI

A

‒ High protein diet

‒ Upper GI bleed (stomach, proximal duodenum)

‒ Increased catabolism

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15
Q

how will increased protein in the upper GI effect BUN

A

↑ production of BUN → ↑ serum BUN

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16
Q

liver insufficiency effect on BUN

A

↓ production of BUN → ↓ serum BUN

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17
Q

renal resorption of BUN

A

Passively resorbed in the proximal tubules (~50%)

Actively resorbed in the collecting tubules (~10%)

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18
Q

T/F Resorption of BUN varies with rate of flow thru tubules.

A

true
Slow flow rate, more BUN resorbed → ↑ serum BUN

Fast flow rate, less BUN resorbed → ↓ serum BUN

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19
Q

T/F Ruminants & horses have unique microflora that allow for GI excretion of BUN

A

true

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20
Q

how do you predict renal disease in ruminants and horses

A

Correlate changes in BUN with changes in CREA and USG

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21
Q

where can decreases in BUN can happen

A

Pre-renal

Renal

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22
Q

Pre-Renal causes of decreased BUN

A

↓ urea production

Intestinal loss of proteins

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23
Q

causes of ↓ urea production

A

Decreased amino acid delivery to liver
− Decreased protein in diet
− Portosystemic shunt (PSS)

Hepatic insufficiency (>80% loss)

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24
Q

causes of intestinal loss of proteins

A

Monogastric species (protein-losing enteropathies)

Horses and Cattle
– Blood urea excrete into saliva & goes to the rumen
– Rumen microflora create amino acids
– Urea is lost in the creation of proteins
(Results in a net protein gain and BUN loss.)

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25
Q

renal causes of decreased BUN

A

Decreased water resorption in proximal convoluted tubules
‒ ↑ GFR (ie, IVF diuresis)
‒ ↑ tubular flow (ie, osmotic diuresis)

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26
Q

Osmotic Diuresis mechanism

A

↑ urine osmolality pulls H2O into urine: ↑ urine volume and ↑ tubular flow

With ↑ tubular flow, ↓ time to resorb BUN → ↓ [BUN]

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27
Q

in what condition is osmotic diuresis common

A

diabetes

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28
Q

concentration of BUN is dependent on

A

Dietary protein

Liver function

Glomerular filtrate rate

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29
Q

T/F creatinine has a constant rate of production

A

true: Produced by endogenous muscle catabolism, rate of production is proportional to muscle mass

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30
Q

T/F creatine is resorbed by the kidney

A

false

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31
Q

what releases CREA into plasma

A

muscle cells

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32
Q

why is CREA and excellent indicator of GFR

A

Filtered by the glomerulus

Not resorbed by the renal tubules

Excreted unchanged by kidneys

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33
Q

increased plasma levels of CREA implies…

A

a decrease in GFR

possibly altered nephron function

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34
Q

decreased CREA

A

not clinically significant

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35
Q

SDMA increases with…

A

~40% loss of renal tubular function

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36
Q

Symmetric dimethylarginine (SDMA)

A

Released into circulation by all nucleated cells

Filtered by the glomerulus

Excreted almost exclusively by the kidneys (≥90%)

Not impacted by extrarenal factors (esp. lean body mass)

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37
Q

interpreting SDMA

A

Increases in SDMA suggest renal tubular disease

Interpret alongside history, clinical signs, PE findings, other markers of renal injury

ALWAYS COME BACK TO YOUR PATIENT.

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38
Q

clinical use of SDMA

A

monitoring

management

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39
Q

if SDMA is increased and CREA is normal:

A

Does your history, C/S, and/or PE findings support renal disease?

Rule out all other causes of ↓ GFR besides RF: Pre-renal, Renal, Post-renal

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40
Q

Urine Specific Gravity

A

an estimate of urinary concentrating capacity

Kidney’s Ability to Conserve Water!!!

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41
Q

run a USG when…

A

Suspected renal disease

Geriatric wellness

Hx of PU/PD

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42
Q

2 parts of the kidney are used to concentrate and/or dilute urine

A

The thick ascending Loop of Henle

The collecting tubule via ADH (Vasopressin)

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43
Q

kidneys ability to conserve water is dependent on

A

33% functional nephrons

Production & responsiveness to ADH

Concentration gradient

  • Medullary hypertonicity
  • Production of urea
  • Production of aldosterone
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44
Q

urine dilution

A

Remove osmoles

Minimize H2O resorption

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45
Q

minimum concentrating capacity in dehydration for a dog

A

1.030

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46
Q

minimum concentrating capacity in dehydration for a cat

A

1.035

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47
Q

minimum concentrating capacity in dehydration for bovine/equine

A

1.025

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48
Q

range of minimal concentration (ROMC)

A
  1. 013-1.030 Dog
  2. 013-1.034 Cat
  3. 013-1.024 Equine, Ruminants, Porcine
49
Q

urine specific gravity should always be interpreted with…

A

patients hydration status

50
Q

why is creatinine is a better indicator of GFR than BUN

A

BUN is resorbed in the kidney

Creatinine is continually and consistently produced by muscle

Creatinine is not resorbed by the kidney

51
Q

polyuria

A

Inability to concentrate urine

Implies loss of ~ 66% of functional renal mass

Low specific gravity (isosthenuric 1.007-1.013)

52
Q

DDx for polyuria

A

Renal

  • Renal failure
  • pyelonephritis

Extra-renal

  • Diuresis
  • Medullary washout
  • Endocrine (diabetes, hyperadrenocorticism)
  • Pyometra
53
Q

Azotemia is due to

A

retention of nitrogenous waste products in blood

implies 75% loss of renal function

54
Q

3 categories of azotemia

A

pre-renal

renal

post-renal

55
Q

what will you see with pre-renal azotemia

A

↑ BUN, +/- ↑ CREA, ↑ SpGr

56
Q

DDx of pre-renal azotemia

A

Decreased renal blood flow leads to ↓ GFR (dehydration!! shock, ↓cardiac output)

Increased urea production (upper GI bleed, high protein diet, ↓ ruminal motility)

57
Q

pre-renal azotemia: Decreased renal blood flow leads to ↓ GFR- analytes effected

A 
2 renal analytes affected by ↓ GFR
   - BUN
   - CREA
Other analytes affected by ↓ GFR
   - Phosphorus (increases)
   - Magnesium (increases)
58
Q

what happens in a dehydrated animal with normal renal function

A

urine volume is decreased (less blood = less urine)

urine specific gravity is increased (concentrated urine)

59
Q

T/F persistently decreased blood flow will cause renal damage

A

true

60
Q

why is there increased urea production with pre-renal azotemia

A

Liver takes amino acids & makes urea

Urea moves into blood → measured as BUN

61
Q

sources of amino acids

A

GI tract

  • Upper GI bleed
  • High protein diet
  • Ruminants: ↓ ruminal motility

Endogenous protein catabolism (starvation, cachexia, neoplasia)

62
Q

causes of increased CREA in pre-renal azotemia

A

Increased muscle mass

Neonatal foals
– Dams with dysfunctional placentas; prevents normal clearance of fetal CREA
– ↑ CREA resolves within a few days

63
Q

renal azotemia

A

↑ BUN, ↑ CREA, ↓ SpGr

64
Q

renal azotemias result in

A

↓ GFR
– Increased BUN
– Increased CREA
– Increased PHOS

Loss of the kidney’s concentrating ability
– Isosthenuria (1.008-1.012)
- Increased water loss, even in a de-H2O animal
- Implies polyuria

65
Q

Causes of renal azotemia =renal damage! DDx:

A 
infectious
toxins
hypoxia
neoplasia
congenital (hypoplasia or aplasia)
66
Q

T/F An animal with azotemia and inappropriately low USG is always in renal failure

A

false

67
Q

other causes of azotemia and inappropriately low USG (besides renal failure)

A

Imbalances in electrolyte metabolism, endocrine function, or drug effects:

  • Calcium
  • Diabetes insipidus
  • Endocrine: cortisol, glucose
  • Fanconi syndrome
  • Diuresis
68
Q

Post-renal Azotemia

A

↑ BUN, ↑ CREA, variable SpGr

69
Q

causes of post-renal azotemia

A

Obstruction of urinary outflow
– Urolithiasis in castrated males
– Uroabdomen (urine leaks into peritoneal cavity): trauma, urolithiasis

70
Q

T/F polyuria occurs before azotemia

A

True:
− Polyuria: ~66% nephron loss
− Azotemia: ~75% nephron loss

71
Q

origin of azotemia is determined by…

A

SpGr
− Prerenal azotemia: ↑ SpGr
− Renal azotemia: ↓ SpGr
− Postrenal azotemia: Variable SpGr (use clinical signs)

72
Q

differentiating azotemias: pre-renal

A

Are there other signs of dehydration?

Is there a reason for this patient to bleed? (GI ulcer, upper GI bleed, coagulopathy)

Is the patient on a ↑ protein diet?

73
Q

T/F Azotemia + Isosthenuria = Renal disease until proven otherwise

A

true

74
Q

what is the exception to isosthenuria + azotemia=renal disease

A

cats: can maintain some concentrating capacity with renal failure

75
Q

differentiating azotemias: post-renal

A 
Look to your signalment and PE findings:
−Castrated males (more frequent)
−Straining to urinate
−Large turgid bladder
−Distended abdomen (uroabdomen)
76
Q

T/F healthy dogs may have a measurable protein concentration

A

true: mostly albumin

77
Q

Urine protein concentration

A

Measurement by reagent strip

Measures albumin!

78
Q

3 types of proteinuria

A

Prerenal (increased protein in blood)

Renal (glomerular & tubular)

Postrenal (hemorrhagic / inflammatory)

79
Q

pre-renal proteinuria

A 
Increase in a small protein in blood
• Paraproteinuria (Bence-Jones)
• Hemoglobinuria
• Myoglobinuria
• Post-colostral proteinuria
80
Q

renal proteinuria

A

Glomerular proteinuria
– Hypoalbuminemia
– Disease damages filtration barrier

Tubular proteinuria
– Normal or increased serum ALB (e.g. no hypoalbuminemia)
– Usually associated with acute or congenital renal diseases
– Proximal tubules defective – filtered proteins not resorbed

81
Q

post-renal proteinuria

A

Hemorrhagic / Inflammatory (will see pyuria)

82
Q

when do we use UPCR

A

Don’t have hemorrhage or pyuria, not febrile, no history of seizure- nothing to points in the direction its going on before the kidney

Differentiates between leaking of glomerular proteins and leaking of tubular proteins: albumin is one way but can be more subtle than that

83
Q

what does UPCR do

A

Estimate quantity of urinary protein excreted/ day

84
Q

T/F glomerular proteinurias tend to be more severe

A

true

85
Q

hypercalcemia in renal failure

A

Impairs urine concentrating ability causing primary PU
- affects ADH receptors

Commonly leads to mineralization of renal tubules → nephronal(kidney) dysfunction

86
Q

T/F Most of the time, hypercalcemia causes kidney disease

A

true

87
Q

calcium levels in renal failure

A

Dogs, cats & cattle: mild hypocalcemia
– ↓ 1,25-dihydroxy vitamin D

Horses: hypercalcemic (diet & excretion)

88
Q

hyperphosphatemia in renal failure

A

GFR is

89
Q

T/F hyperphosphatemia is not as common in cattle and horses

A

true:
- horses tend to lose from the gut
- cattle: Salivary Phos excretion > renal Phos excretion

90
Q

T/F cattle with renal failure can be hypochloremic

A

true

91
Q

why do you see a metabolic acidosis with severe renal disease

A

↑ urinary loss of HCO3

↓ tubular secretion of H+ ions

92
Q

Normokalemia

A

– Potassium is often normal in CRF

– Increased tubular secretion prevents hyperkalemia

93
Q

Hypokalemia

A

– Uremic animals often eat less → ↓K intake

– Hypokalemic nephropathy in cats
- Pathogenesis unknown, likely multifactorial

94
Q

Hyperkalemia

A

– Associated with oliguria/ anuria

– Life-threatening in ARF and/or post-renal conditions

95
Q

Uroabdomen and Electrolyte Imbalances: Dogs, cats & newborn foals

A

– ↑ K, PO4

– ↓ Na, Cl

An ↑K and ↓Na occurs with several diseases. Uroabdomen = one ddx

96
Q

Uroabdomen and Electrolyte Imbalances: cattle

A

– Hyperkalemia does not occur

–Excess potassium excreted in saliva

97
Q

when is peritoneal [CREA] diagnostic for uroperitoneum

A

Peritoneal [CREA] 2x serum [CREA]

98
Q

why is [CREA] used as an indicator of uroperitoneum

A

CREA takes longer to move from peritoneal urine into blood (large molecule)

smaller molecules move more quickly

99
Q

what are major diagnostic indicators of uroabdomen?

A

Hyperkalemia, hyponatremia (↑K, ↓Na)

Peritoneal creatinine greater than 2x higher than serum creatinine

100
Q

which electrolytes move into plasma quickly?

A

Urea and K+ move into plasma quickly, plasma [ ] increases

101
Q

which electrolytes move into urine quickly?

A

Na+ and Cl- move into urine quickly, plasma [ ] decreases

102
Q

presentation of ARF

A

Patient: Any signalment

History: Acute onset of clinical signs (e.g. GET SICK FAST.)

103
Q

physical exam AFR

A

Patients usually have a good BCS (vs. CRF patients)

GI - anorexia, vomiting, diarrhea, halitosis (NH3)

Renal - oliguric to anuric

Neuro - depressed → obtunded → nonresponsive → seizures

104
Q

causes of ARF

A

Many!!

Commonly associated w/ toxicants, renal ischemia, or infection
– i.e., things that damage the kidneys swiftly! (antifreeze poisoning)

105
Q

features of ARF

A

Marked decrease in GFR leading to azotemia

May be reversible or irreversible

106
Q

Bloodwork findings ARF

A

Azotemia (fast increase with ARF)

+/- Hyperkalemia & Acidemia

  • Impaired excretion of K+ and H+ leads to metabolic acidosis
  • Failure to recapture HCO3
107
Q

Urinalysis: ARF

A

‒ Oliguria or anuria (abrupt ↓GFR)

‒ Urine SpGr is variable

‒ +/- proteinuria

‒ +/- cellular casts

108
Q

CRF presentation

A

Patient: Usually geriatric (but not always), frequently cats

History: Slow onset of clinical signs

109
Q

CRF physical exam

A

Patients usually have a poor BCS (thin, cachexic)

GI - anorexia, vomiting, diarrhea, halitosis (NH3)

Renal - polyuric

Neuro - depressed

CV - hypertension

110
Q

features of CRF

A

Irreversible kidney injury

Renal function is inadequate to maintain patient health

Decreased GFR

Azotemia

Isosthenuria

111
Q

CRF Bloodwork and Urinalysis: GFR 20-25% normal

A

Nonregenerative anemia (no EPO production)

Dehydration
- kidneys cannot regulate body H2O

Azotemia

+/- Hyperphosphatemia (85%)

Metabolic acidosis
- kidneys cannot regulate electrolyte and A/B

Normokalemia to Hypokalemia

Polyuria, isosthenuria

112
Q

CRF Bloodwork & Urinalysis: GFR less than 5% normal=end stage renal failure

A

Nonregenerative anemia

Marked dehydration

Marked azotemia (patients are uremic)

Hyperphosphatemia

Metabolic acidosis

Hyperkalemia

Isosthenuria

Oliguria to anuria

113
Q

Glomerular Nephropathy

A

Renal glomerular damage:

1) Immune complex deposition
2) Amyloid deposition

114
Q

GN causes:

A

Retraction of podocytes

Loss of selective permeability of the glomerular basement membrane

115
Q

GN allows filtration of larger negatively charged proteins causing

A

proteinuria

hypoproteinemia

116
Q

GN laboratory findings

A

Mild to marked hypoproteinemia
‒ Hypoalbuminemia
‒ Normoglobulinemia

Moderate to marked proteinuria (albuminuria)

+/- evidence of renal insufficiency (azotemia, isosthenuria)

117
Q

albumin decreases on its own with…

A

Albumin decreases on it own with protein losing nephritis (glomerular nephropathies), vasculitis, liver failure, and INFLAMMATION!!!!

118
Q

Nephrotic Syndrome:

A

Protein-losing nephropathy leading to abdominal transudation

119
Q

what 5 things need to be present to Dx nephrotic syndrome

A
  1. Glomerular disease
  2. Hypoalbuminemia - Leaky glomeruli (PLN)
  3. Hypercholesterolemia - Poorly understood
  4. Edema/ abdominal effusion - Loss of plasma oncotic pressure
  5. Hypercoagulable state- Loss of antithrombin

RUSVM Clin Path (11 decks)

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