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ACVIM General Old Questions 2 > Renal > Flashcards

Renal Flashcards

1
Q

What is the equation for urinary clearance?

A

C = ([U] x urine flow)/[P]

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2
Q

What is the equation for urinary excretion?

A

[U] x Urine Flow

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3
Q

What is the pattern for metabolic acidosis?

A 
CO2 + H2O: Decreased (Resp. comp)
H+: Increased
HCO3-: Decreased*
Resp. Comp.: Hyperventilation
Renal Comp: -
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4
Q

What is the pattern for metabolic alkalosis?

A 
CO2 + H2O: Increased (Resp. comp)
H+: Decreased
HCO3-: Increased*
Resp. Comp.: Hypoventilation
Renal Comp: -
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5
Q

What is the pattern for respiratory acidosis?

A 
CO2 + H2O: Increased*
H+: Increased
HCO3-: Increased
Resp. Comp.: -
Renal Comp: Increased H+ Excretion, Increased HCO3- Reabsorption
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6
Q

What is the pattern for respiratory alkalosis?

A 
CO2 + H2O: Decreased*
H+: Decreased
HCO3-: Decreased
Resp. Comp.: -
Renal Comp: Decreased H+ Excretion, Decreased HCO3- Reabsorption
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7
Q

What is the equation for strong ion difference?

A

[Strong cations] - [Strong anions]
[Na + K + Ca + Mg] - [Cl + Lactate]

*NOT affected by albumin concentration → anion gap is!

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8
Q

What occurs with an increased strong ion difference?

A

Metabolic Alkalosis

*Increased Na or Decreased Cl

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9
Q

What occurs with a decreased strong ion difference?

A

Metabolic Acidosis

*Decreased Na or Increased Cl

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10
Q

Tubular Reabsorption:

  1. Filtered only
  2. Filtered with partial reabsorption
  3. Filtered with complete reabsorption
  4. Filtered and secreted
A
  1. Inulin and creatinine
  2. Electrolytes
  3. Amino acids and glucose
  4. Organic acids and bases
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11
Q

Describe renal blood flow. Why is this unique?

A

Renal artery → interlobar → arcuate → interlobar → afferent → glomerular capillaries → efferent → peritubular capillaries → interlobar → arcuate → interlobar → renal vein

*Unique because it has 2 capillary beds

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12
Q

What is the MOA of ADH?

A

Goes to distal/collecting ducts → V2 receptors → adenylyl cyclase → cAMP → Protein kinase A → phosphorylation of membrane proteins → transient placement of aquaporin channels in the membrane → permeable to water

*Released in response to osmoreceptors in the anterolateral hypothalamus near the supraoptic nuclei

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13
Q

What is the net filtration pressure equation?

A

NFP = P(GC) - P(BC) - π(GC)

P = hydrostatic pressure
π = oncotic pressure
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14
Q

What is responsible for RAAS inhibition?

A

Atrial Natriuretic Peptide (ANP)

- Comes from cardiac atrial muscle fibers

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15
Q

Approx. 90% of the filtered glucose is reabsorbed by ____ in the ____ part of the proximal tubule

A
  1. SGLT2

2. Early (S1)

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16
Q

Which portions of the nephron are impermeable to water?

A
  1. Thick ascending loop of Henle

2. Early distal tubule

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17
Q

Where do the following act (segment & receptor)?

  1. Carbonic anhydrase inhibitors
  2. Thiazide diuretics
  3. Loop diuretics
  4. K sparing diuretics
A
  1. Early proximal tubule → inhibit HCO3 reabsorption
  2. Early distal tubule → inhibits Na-Cl cotransporter
  3. Thick ascending loop of Henle → inhibit Na-K-2Cl cotransporter
  4. Late distal tubule → aldosterone receptor antagonist
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18
Q

Where is Na reabsorbed in the nephron?

A

*99% filtered Na is reabsorbed

  1. Proximal tubule - 65% (Active)
  2. Thin ascending LoH - 7% (Passive)
  3. Thick ascending LoH - 20% (Active)
  4. Distal tubule - 8% (Active)
  5. Collecting duct - 3% (Active)
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19
Q

Where is K reabsorbed/secreted in the nephron?

A
  1. Proximal tubule - 67% reabsorbed
  2. Thick ascending LoH - 20% reabsorbed
  3. Distal tubule & collecting duct → reabsorbs or secretes based on dietary K
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20
Q

Where is phosphate reabsorbed in the nephron?

A

*85-90% of filtered phosphate is reabsorbed

  1. Proximal tubule - 75-80%
  2. Distal convoluted tubule - 10%
  3. Loop of Henle and collecting tubules - <1%
  • ~15% of filtered load is excreted in the urine
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21
Q

Where is the majority of Ca reabsorbed in the nephron?

A

*99% of filtered Ca is reabsorbed

  1. Proximal tubule - 65% (active and passive)
  2. Thick LoH - 25-30% (passive)
  3. Distal tubule and collecting duct - 4-9% (active)
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22
Q

How does PTH influence the phosphorous balance by the kidneys?

A

Decrease transport mechanism for phosphate by the renal tubules → more is lost in the urine

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23
Q

Magnesium competes with ___ in the thick ascending loop for reabsorption

A

Calcium

*Hypercalcemia causes an increase in Mg excretion

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24
Q

The corticopapillary osmotic gradient occurs in the presence of (high/low) ADH and is mostly composed mostly of ___ and ___.

A
  1. High

2. NaCl and Urea

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25
Q

Interpret:

  1. TF/P = 1
  2. TF/P < 1
  3. TF/P > 1
A
  1. There has either been no reabsorption or reabsorption is exactly proportional to water
  2. Reabsorption is greater than reabsorption of water → tubular fluid concentration < plasma concentration
  3. Reabsorption is less than reabsorption of water → tubular fluid concentration > plasma concentration (there has been no secretion)
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26
Q

What is the consequence of no ADH in terms of urine concentrating ability?

A

Cells of the late distal tubule and collecting duct are impermeable to H2O

Urine is dilute

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27
Q

Where is free H2O produced in the nephron

A

Diluting segments → TAL and early distal tubule

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28
Q

Where is ADH produced and stored?

A
  1. Hypothalamus - supraoptic nuclei (majority)

2. Posterior pituitary

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29
Q

At what positions do the liver and kidney hydroxylate vitamin D?

A
  1. Liver → 25 → “25-OH-D (Calcidiol)”

2. Kidney → 1 → “1,25(OH)2-D (Calcitriol)”

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30
Q

What substances are used to measure:

  1. ECF
  2. Plasma
  3. Intersitial Fluid
  4. ICF
A
  1. Sulfate, Inulin, Mannitol
  2. Evans Blue, RISA (Radioiodinated serum albumin)
  3. Measure indirectly (ECF-plasma)
  4. Measured indirectly (TBW-ECF)
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31
Q

How is renal plasma flow measured?

A
  1. PAH
    - Filtered and secreted by renal tubules
    - Clearance of PAH measures effective RPF but underestimates true RPF by ~10%
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32
Q

What is the equation to calculate renal blood flow?

A

RBF = RPF/(1-HCT)

RPF = PAH clearance

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33
Q

What is the equation used to calculate GFR (starling equation)? What does a (+) value indicate?

A

GFR = Kf [(P(GC)-P(BS)) - (π(GC) - π(BS)]

(+) = filtration is favored

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34
Q

Where is glucose reabsorbed in the nephron? How is this accomplished?

A
  1. Early proximal tubule

2. Na-Glucose co-transport

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35
Q

What is the MOA of ANP in RAAS inhibition?

A
  1. Stimulus → dilution of the atria
  2. Effects
    - Inhibit renin release
    - Inhibit action of angiotensin II
    - Inhibits Na reabsorption
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36
Q

What is the plasma osmolality equation?

A

2(Na+K) + Glucose/18 + BUN/2.8

Osmolality = # of osmoses per kilogram of solvent

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37
Q

How does ECF volume affect proximal tubular reabsorption

A
  1. ECF volume contraction → increase reabsorption
    - Peritubular capillary protein increases = increased π(capillary) = decreased P(capillary) = increase in proximal tubular reabsorption
  • Opposite is also true
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38
Q

What are the mechanisms of K reabsorption and secretion in the distal tubule and collecting duct?

A
  1. Reabsorption → α intercalated cells
    - H/K ATPase countertransport
  2. Secretion → Principal cells
    - Basolateral membrane: K actively transported into cell via Na/K pump
    - Luminal membrane: K passively secreted into lumen through K channels
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39
Q

How does ADH affect urea regulation?

A

Acts on UT-A1 and UT-A3 transporters

Increases urea in the interstitial → increases concentrating ability

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40
Q

What stimulates ADH secretion?

A
  1. Increase plasma osmolality
    - Osmoreceptors in anterior hypothalamus
  2. Decrease atrial pressure/blood volume
    - Baroreceptors
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41
Q

What is the relationship between BUN and serum creatinine in prerenal azotemia? Why?

A
  1. BUN increases more than creatinine

2. Hypovolemia increases urea reabsorption in the proximal tubule

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42
Q
  1. How are weak acid and weak base forms affected by:
    a. acidic urine
    b. alkaline urine
  2. How does this affect their excretion?
A

1a. HA form and BH+ form predominate
1b. A- and B form predominate

2.a. More back diffusion of acid = decrease excretion
Less back diffusion of base = increase excretion
2b. Less back diffusion of acid = increase excretion
More back diffusion of base = decrease excretion

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43
Q

What is the mechanism of phosphate reabsorption in the proximal tubule?

A

Na-Phosphate cotransport

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44
Q

What inhibits phosphorous reabsorption in the proximal tubule? How?

A
  1. PTH
  2. Activates cAMP → inhibits Na-phosphate co-transport
    - Causes phosphaturia and increased urinary cAMP

*FGF23 (fibroblast growth factor) is secreted by bone and also inhibits the Na-phosphate co-transporter

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45
Q

How do the following affect Ca excretion/resorption in the nephron?

  1. Loop diuretics
  2. PTH
  3. Thiazide diuretics
A
  1. Increase excretion in the LoH
  2. Increase reabsorption in the distal tubule
  3. Increase reabsorption in the early distal tubule
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46
Q

Where is magnesium reabsorbed in the nephron?

A
  • 85-90% reabsorbed
  1. LoH - 65% (mostly from thick)
  2. Proximal tubule - 25%
  3. Distal convoluted tubule and collecting duct - <5%
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47
Q

Where does PTH act in the nephron?

A
  1. Thick limb of the LoH

2. Distal convoluted tubule and collecting duct

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48
Q

What are the transport mechanisms for Na in

  1. Early proximal tubule
  2. Distal proximal tubule
A
  1. Cotransporters → glucose, amino acids, phosphate, and lactate
    Countertransport → Na-H exchange linked to HCO3 reabsorption
  2. Reabsorbed with Cl
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49
Q

What are the transport mechanisms for Na in

  1. Thick ascending LoH
  2. Early distal tubule
  3. Late distal tubule
A
  1. Na/K/2Cl cotransporter
  2. Na/Cl cotransporter
  3. Na Channels (stimulated by aldosterone)
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50
Q

What are the different vasopressin receptors?

A
  1. V1A → vascular smooth muscle → vasoconstriction
  2. V2 → collecting ducts → insert aquaporin 2 channels
  3. V3 → anterior pituitary → ACTH release
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51
Q

What causes renal arterioles to

  1. Vasoconstrict
  2. Vasodilate
A
  1. Sympathetic nervous system, angiotensin II
    * Angiotensin II preferentially constricts efferent arterioles at low concentrations to increase GFR
  2. Prostaglandins E2 and I2, Bradykinin, NO, and Dopamine
    * ACEi → dilate efferent arterioles
    * ANP → dilate afferent arterioles
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52
Q

Where is urea reabsorbed in the nephron?

A
  1. Proximal tubule - 50% (simple diffusion)
  2. Thin descending limb - simple diffusion
  3. Collecting ducts - UT1 transporter only in the presence of ADH, otherwise distal tubule and collecting duct are impermeable to urea
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53
Q

What are the different urea transporters?

A
  1. UT-A1: Reabsorption in proximal tubule and collecting duct
  2. UT-A2: Secretion into the think loop of henle
  3. UT-A3: Reabsorption in the collecting duct
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54
Q

Reabsorption of filtered HCO3 occurs primarily in which nephron segment?

A

Proximal tubule

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55
Q

What is the carbonic anhydrase equation?

A

CO2 + H2O -> H2CO3 -> carbonic anhydrase -> H + HCO3

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56
Q

What is the net result of bicarb reabsorption in the proximal tubule?

A
  1. Net reabsorption of filtered HCO3

2. Does not result in net H+ secretion

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57
Q

What regulates reabsorption of filtered HCO3

A
  1. Filtered Load → Increased filtered load = increased HCO3 reabsorption
  2. PCO2 = Increased PCO2 = Increased HCO3 because supply of intracellular H is increased → bases of renal compensation for respiratory acidosis
  3. ECF Volume → ECF expansion = decreased HCO3 reabsorption. ECF contraction = increased HCO3 reabsorption
  4. Angiotensin II = stimulates Na/H exchange and thus increased HCO3 reabsorption, contributes to contraction alkalosis that occurs secondary to ECF volume contraction
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58
Q

In what forms is H+ excreted?

A
  1. Titratable acid (H2PO4)

2. NH4

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59
Q

What determines the amount of H+ excreted as a titratable acid?

A
  1. Amount of urinary buffer (usually HPO4)

2. pK of the buffer

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60
Q

What determines the amount f H+ excreted as ammonium?

A
  1. NH3 synthesized by renal cells

2. Urine pH

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61
Q

How/where is NH3 produces in the kidney? What inhibits this process?

A
  1. Produced in renal cells from glutamine

2. Hyperkalemia inhibits NH3 synthesis

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62
Q

What is the underlying cause of metabolic acidosis?

A

Overproduction/ingestion of acid

OR

Loss of base = decrease in [HCO3]a → acidemia

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63
Q

What are consequences of a metabolic acidosis?

A
  1. Hyperventilation → respiratory compensation
  2. Increased excretion of H as a titratable acid and ammonium
  3. Increased reabsorption of HCO3
  4. In chronic cases → increase NH3 synthesis
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64
Q

What is the underlying cause of a metabolic alkalosis?

A

Loss of [H+]

OR

Gain of base → increase arterial [HCO3] → alkalemia

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65
Q

What are the consequences of a metabolic alkalosis?

A
  1. Hypoventilation → respiratory compensation

2. Increased excretion of HCO3 → filtered load of HCO3 exceeds the kidneys ability to reabsorb it

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66
Q

What is contraction alkalosis?

A

Metabolic alkalosis is accompanied by ECF volume contraction (vomiting) → reabsorption of HCO3 increases due to ECF volume decrease and activation of RAAS → worsens alkalosis

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67
Q

What is the underlying cause of respiratory acidosis?

A

Decreased ventilation and retention of CO2 → increased arterial CO2 → increased H+

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68
Q

How does the kidney compensate for respiratory acidosis?

A
  1. Increased excretion of H+ as titratable acid and ammonium, increased reabsorption of HCO3
    * Aided by increased PCO2 → supplies more H+ to the kidney
    * Takes time, only occurs in CHRONIC cases
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69
Q

What is the underlying cause of respiratory alkalosis?

A

Increased ventilation → loss of CO2 → decreased H+

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70
Q

How does the kidney compensate for respiratory alkalosis?

A

Decreased excretion of excess H, decrease reabsorption of HCO3

*Takes time, only occurs in chronic cases

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71
Q

What are the effects of hypoaldosteronism on the kidney

A
  1. Decrease Na reabsorption
  2. Decrease K secretion
  3. Decrease H secretion
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72
Q

What stimulates the production of erythropoietin? How long does it take for HCT to increase?

A
  1. Epi, Norepi, prostaglandins, and HIF1α

2. 5 days

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73
Q

What happens when the macula dense senses a decrease in the NaCl in the distal tubules

A
  1. Dilates afferent arterioles → increase RBF and GFR

2. Causes renin release from JG cells → RAAS

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74
Q

Where does aldosterone act in the kidney? Where is the primary site of action?

A
  1. Principal cells of distal tubule and collecting duct → increase Na reabsorption, increase K secretion
  2. Intercalated cells of distal tubular and collecting duct → increase H secretion
  3. Thick LoH → increase Na-2Cl-K transporter expression, Increase Cl and Na reabsorption
  • Principal cells of the cortical collecting tubule is the primary site of action
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75
Q

What are the actions of Angiotensin II?

A
  1. Stimulates aldosterone
  2. Constricts efferent and afferent arterioles (via phospholipase C)
  3. Increase Na reabsorption (via adenylyl cyclase)
  4. Increase thirst
  5. Increase ADH secretion
  6. Potentiates post synaptic norepinephrine release
  7. Blunt baroreceptor response
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76
Q

What is the equation for filtration fraction? how much is normally filtered?

A

Filtration fraction = GFR/Renal plasma flow

~20% of plasma

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77
Q

What increases Ca reabsorption in the nephron?

A
  1. Acidosis
  2. Increase PTH
  3. Decrease ECF volume
  4. Increase BP
  5. Increase Vit D3
78
Q

What buffer system is most important

  1. Extracellularly
  2. Tubular fluid
  3. Intracellularly
A
  1. HCO3
  2. Phosphate
  3. Phosphate
79
Q

Hyperaldosteronism acid/base status

A

Metabolic alkalosis → Increase H+ secretion

80
Q

2/3 of filtered H2O is reabsorbed in which part of the nephron?

A

Proximal tubule

81
Q

What is the equation for free water clearance?

A

Urine flow rate - osmolar clearance

Osmolar clearance = (urine osmolarity x urine flow rate)/plasma osmolarity

82
Q

What is nephrotic syndrome?

A
  1. Peripheral edema
  2. Proteinuria
  3. Hypoalbuminemia
  4. Hypercholesterolemia
83
Q

Cats with FIC have increased levels of what?

A
  1. Tyrosine hydroxylate in the hypothalamus

2. Plasma norepinephrine levels

84
Q

What are the diagnostic criteria for renal tubular acidosis?

A
  1. Normal to near normal GFR

2. Hyperchloremic, normal anion gap, metabolic acidosis without GI disease

85
Q

Indications for a renal diet

A
  1. Proteinuric with UPC > 2
  2. Creatinine indicating IRIS stage 2 in cats and stage 3 in dogs
  3. Phosphorous > 4.5
  • Use of a renal diet will more than double survival tiems
86
Q

What are the major side effects of glomerular disease?

A
  1. Edema
  2. Hypertension → 80% of patients
  3. Thromboembolic events → 5-15% of patients
  4. Hyperlipidemia
87
Q

What kind of uroliths can be dissolved?

A

Struvite, cysteine, and urate

88
Q

What % of lyme positive dogs have proteinuria?

A

<2%

95% of lyme seropositive dogs show no signs of illness

89
Q

What are causes of decreased iCa?

A
  1. Alkalosis → important
  2. Lipemia
  3. Increase BP/ECV
  4. Decrease PTH
90
Q

What are the causes of acquired Fanconi syndrome?

A
  1. Gentamycin
  2. Ethelyne glycol toxicity
  3. Primary hypoparathyroidism
91
Q

What are some complications associated with recurrent UTI

A
  1. Polypoid cystitis
  2. Emphysematous cystitis → commonly associated with E. coli
  3. Struvite uroliths
  4. Pyelonephritis
92
Q

What are the indications of underlying glomerular disease?

A
  1. Proteinuria with UPC > 0.5 on more than one occasion
  2. Proteinuria and glomerulotubular imbalance (azotemia with concentrated urine)
  3. Casts are often present
93
Q

How can calcium oxalate stone recurrence be prevented?

A
  1. Potassium citrate

2. Thiazide diuretics

94
Q

What is the treatment of cystine stones?

A

2MPG + Alkaline urine (potassium citrate or bicarb) + protein restriction

95
Q

What are the underlying causes for struvite stones?

A
  1. Develop secondary to UTI with urease producing bacteria → drive development of alkaline urine and ammonium
  2. Staphylococcus and proteus are the most common
96
Q

What are the components of purine stones?

A

Urate and xanthine

97
Q

How common are calcium oxalate stones?

A
  1. 40% of all canine uroliths
  2. Male predisposition
  3. More common in small breeds
98
Q

What increases the risk of calcium oxalate stones?

A
  1. Hypercalcinuria
    - Due to increase intestinal reabsorption, increased bone resorption, or primary renal Ca leak
  2. Common with hyperparathyroidism
99
Q

How are purine stones treated?

A
  1. Liver abnormalities → removal
  2. Genetic abnormalities → dissolve
    - Protein restricted diet with BUN < 10
    - Dilute urine to < 1.015
    - Alkaline pH > 7.0
    - Xanthine oxidase inhibitors (allopurinol)
100
Q

Describe purine metabolism

A

Purine catabolism → hypoxanthine → xanthine oxidase → xanthine → xanthine oxidase → uric acid → urate oxidase → allantoin

101
Q

What are calcium phosphate uroliths composed of and what disease process are they associated with?

A
  1. Hydroxyappetite

2. Hyperparathyroidism (30-40% will develop)

102
Q

How common are uroliths in cats?

A

10-15% of cats with lower urinary signs with uroliths

103
Q

What are the most common uroliths in the cat?

A
  1. Calcium oxalate - similar process as dogs

2. Struvite

104
Q

What % of intact male dogs have BPH?

105
Q

What is the treatment of choice for BPH?

A

Castration

  • 50% reduction in 3 weeks
  • 75% reduction in 3 months
106
Q

What is the equation for free water deficit?

A

Weight(present) X ((PNA(present)/PNA(previous)) - 1)

  • If you dont know the previous Na, assume high end of normal (145)
107
Q

Dogs with PLE have altered amounts of which amino acids?

A
  1. Asparagine
  2. Glycine
  3. Proline
  4. Serine
  5. Tyrosine
108
Q

What are the results of glomerular hypertension?

A
  1. Increased single nephron GFR

2. Enlarged radii of the pores of the filtration membrane

109
Q

Survival time for azotemic nephrotic syndrome

110
Q

When should immunosuppressive therapy be considered for dogs with glomerular disease?

A
  1. Serum creatinine > 3.0
  2. Azotemia is progressive
  3. Hypoalbuminemia < 2.0
  • Assess response to therapy in 8-12 weeks
111
Q

What is the most powerful stimulus for aldosterone?

A

Hyperkalemia

112
Q

What would you expect in a patient with increased bicarb and decreased K

A

Paradoxical aciduria

113
Q

What are the differentials for hyperosmotic urine?

A
  1. SIADH
  2. H2O Deprivation
  3. Volume depletion
114
Q

What produces prostaglandins and what do they do?

A
  1. PGE2 produced by type 1 medullary interstitial cells

2. Increase cortical blood flow and decreased medullary blood flow

115
Q

Effects of loop diuretics in the context of AKI

A
  1. Increase urine production
  2. Decrease energy requirements without increase GFR
    * Work in 20-60 min
116
Q

Mechanisms of reduced GFR in AKI

A
  1. Obstruction - sloughed tubular cells block lumen
  2. Vasoconstriction - due to sub endothelial cell injury which promotes endothelia production
  3. Leaking in the tubules allows filtrate to diffuse back into the interstitium
117
Q

What are the most common causes of CKD in dogs

A
  1. Tubulointerstitial nephritis (60%)
  2. Glomerulonephritis (30%)
  3. Amyloidosis (7%)
118
Q

What is the difference between type 1 and type 2 renal tubular acidosis?

A
  1. Type 1 → Distal, cannot secrete H+ by intercalated cells

2. Type 2 → Proximal, cannot reabsorb bicarb

119
Q

How do you treat membrinoproliferative glomerulonephritis in the dog?

A
  1. Aspirin → because platelet activation and TXA2 induced vasoconstriction would promote progression
  2. Glucocorticoids → for immunosuppression
120
Q

What is the underlying cause for hereditary nephritis?

A

Collagen IV deficit results in leaky glomerular basement membrane

121
Q

What is the most common form of glomerular disease in the dog?

A

Membranoproliferative glomerulonephritis

*Occurs commonly secondary to antibody complexes from Borrelia burgdorferi → immune complexes deposit on subendotheilial glomerular basement

122
Q

How is amyloidosis different in Shar Peis?

A
  1. Familial form
  2. Medulla is most common location for deposition → glomerulus may not be involved
  3. 40% have proteinuria
  4. Often have history of Shar Pei fever
123
Q

Routin UTI screening is recommended for cats with which risk factors?

A
  1. Recent catheterization
  2. PU surgery
  3. Diabetes mellitus
  4. Renal failure
  5. Hyperthyroidism
124
Q

What is the treatment for struvite stone?

A

Antibiotics + acidic urine

Takes ~3 months to dissolve

125
Q

What is the treatment for urate stones?

A

Allopurinol + alkaline urine (bicarb or potassium citrate) + protein restriction

126
Q

What is the treatment for calcium oxalate stones?

A

Surgery is the only option!

They will not dissolve!

127
Q

How frequently do calcium oxalate stones recur?

A

Dogs: 50% within 3 years

128
Q

How common are struvite stones?

A

40% of canine uroliths

129
Q

What are the most common breeds for purine stones? Why?

A
  1. Dalmations and Bulldogs
  2. Altered purine metabolism → inability to transport urate into the liver for breakdown by uricases into the more soluble solution

*Can also occur in dogs with shunts

130
Q

How do you prevent purine uroliths?

A

Lower protein diet that promotes dilute urine

Vegetarian diets are a good choice

131
Q

What is the underlying cause of cystine stones?

A
  1. Uncommon
  2. Due to proximal tubular defect in cystine reabsorption
  3. Recurrence is common
132
Q

How are struvite uroliths different in the cat?

A

Found in STERILE urine with an ALKALINE pH

Can dissolve in 1 months with an acidifying diet

133
Q

What are the two forms of FIC? Which is the most common?

A
  1. Ulcerative → 10%

2. Non-Ulcerative → 90%, very common

134
Q

How does FIC cause obstruction?

A
  1. Urethral plugs (60%)

2. Urethrospasm (30%) → functional obstruction

135
Q

What kind of crystals form in FIC?

A
  1. Albumin and struvite

* Struvite associated with increased pH caused by inflammation

136
Q

What is the most common cause of urinary incontinence in female dogs?

A
  1. Urethral sphincter mechanism incompetence
    - Develop increased collagen and decreased muscle fibers
  2. Detrusor instability is a less common cause
137
Q

How is urinary incontinence treated in dogs?

A
  1. α adrenergic agonists → improves tone
    - Phenylpropanalomine (90% effective)
  2. Estrogen → Increased # of α receptors
    - Estrogen 50% effective
    * Can be used together
138
Q

What is the most common causative agent for acute bacterial prostatitis?

A

E. coli (70%)

139
Q

Dogs with acute bacterial prostatitis are usually (symptomatic/asymptomatic)

A

Symptomatic

140
Q

Treatment of choice for acute bacterial prostatitis?

A
  1. Neutering to resolve BPH
  2. Antibiotics for 5-7 days prior to surgery
    - TMS or enrofloxacin

*If abscess is present, drainage important for healing and needs 6 weeks of antibiotics

141
Q

Dogs with chronic prostatitis are (symptomatic/asymptomatic)

A

Asymptomatic

142
Q

Nephrogenic diabetes insipidus is often secondary to what?

A
  1. V2 receptor interference

- Drugs, Endotoxins, or Electrolyte Disorders

143
Q

At what point do neurologic signs associated with hypernatremia develop?

144
Q

Causes of false positive proteinuria on dipstick

A
  1. Urine pH >= 7.5

2. Highly concentrated urine

145
Q

What % of proteinuria dogs with bacteruria, pyuria, and lower urinary tract disease would have missed bacterial growth if cultured?

A

1.8% → Grimes 2020 JVIM

146
Q

How is colchicine metabolized?

A

Cytochrome p450

*This is an MDR1 substrate

147
Q

What are the effects of using an ACEi?

A
  1. Dilation of efferent arterioles
    - Decrease GFR
    - Decrease proteinuria
148
Q

What is the goal when starting an ACEi

A
  1. Achieve normal UPC or decrease UPC by 50%

* Wait 1 month before rechecking

149
Q

Which receptor(s) is blocked by angiotensin II receptor blockers?

A
  1. Angiotensin II type 1 receptors (AT1)

- Do not block AT2

150
Q

What are the roles of the following receptors?

  1. AT1
  2. AT2
A
  1. Produce glomerular hypertension and activation of pro-inflammatory, profibrotic pathways
  2. Mediate renoprotective effects → vasodilation, natriuresis, inhibit renin, anti-inflammatory, anti-ischemic, and anti-fibrotic
151
Q

What is indicated by a metabolic acidosis with normal anion gap?

A
  1. Cl increased

- Occurs with diarrhea or renal tubular acidosis

152
Q

Urinary fractional excretion <1% is most consistent with what?

A

Dehydration/Prerenal azotemia

153
Q

What is a risk of a DDVAP trial in a dog with psychogenic polydipsia?

A

Hyponatremia

154
Q

What are the criteria for central diabetes insidious?

A
  1. Dilute urine despite strong osmotic stimuli for ADH release
  2. Absence of renal disease
  3. Increase osmolality following ADH administration
155
Q

How are calcium oxalate stones prevented?

A

Adequate hydration

156
Q

What drug increases the osmolar gap?

157
Q

Cats with membranous glomerulonephritis have improved survival if?

A
  1. IgG or C3 deposition → compared to those with IgM or IgA or higher stage
158
Q

Which enzyme (other than ACE) can produce angiotensin II?

159
Q

Which type of RTA has:

  1. Alkaline urine despite metabolic acidosis
  2. Lower fractional excretion of HCO3
  3. Higher fractional excretion of HCO3
A
  1. Type 2
  2. Type 1
  3. Type 2
160
Q

Effect of diltiazam in context of AKI

A

May help to stabilize membrane and improve renal blood flow

161
Q

3 most common causes of AKI

A
  1. Toxic
  2. Ischemic
  3. Infectious
162
Q

Effects of mannitol in context of AKI

A
  1. Increase GFR
  2. Relieve tubular obstruction
  3. Decrease local energy requirements
163
Q

What are the consequences of decreased oxygen supply in the context of AKI

A
  1. Inability to power Na-K ATPase → cellular swelling → death
164
Q

AKI is considered to be a creatinine increase of ___ from baseline

A

> 0.3 mg/dl

165
Q

Pyelonephritis is most commonly associated by gram (+/-). Which organism is most common?

A
  1. 75% are gram -

2. 40% of all UTIs caused by E. coli

166
Q

AKI: Most common toxins

  1. Dog
  2. Cat
A

In order of frequency

  1. Ethelyne glycol, NSAID, Vit D3, Aminoglycosides
  2. Ethelyne glycol, Vit D3, Lilies
167
Q

What kind of abs is recommended for the best renal penetration?

A
  1. Fluoroquinolones

* Potentiated pencilling have moderate renal penetration

168
Q

If hypokalemia refractory to K supplementation, consider ___ supplementation

169
Q

Consequences of mannitol administration for AKI in

  1. Dehydrated patient
  2. Overhydrated patient
A
  1. Worsen intracellular dehydration

2. May drive pulmonary edema

170
Q

What is the only acute way to decrease phosphorous (AKI)

A

Dialysis

*Phosphate binders prevent absorption from food

171
Q

Definition of CKD

A
  1. Kidney damage that has existed for >3 months with or without decrease GFR

OR

  1. Decrease GFR by >50% for >3 months
172
Q

Most common causes of CKD in cats

A
  1. Tubulointerstitial nephritis (70%)
  2. Glomerulonephritis (15%)
  3. Lymphoma (10%)
  4. Amyloidosis (2%)
173
Q

What are the characteristics of a renal diet?

A
  1. Low protein
  2. Low phosphorous
  3. High omega 3
174
Q

Hypertension promotes progressive CKD by

A

Worsening proteinuria

175
Q

What is the most common type of glomerular disease in the dog? What are its subtypes? The cat?

A
  1. Membranoproliferative glomerulonephritis
    - Type 1: Subendothelial IC deposition
    - Type 2: Intramembranous IC deposition (uncommon)
    - Type 3: Subepithelial IC deposition
  2. Cat: Membranous glomerulonephritis
176
Q

What is Fanconi Syndrome?

A

A syndrome of inadequate reabsorption in the proximal tubule

  • Inherited in 10-30% of Basenji’s
  • Often develop hyperchloremic metabolic acidosis from loss of bicarbonate
177
Q

What are ACEi used to treat glomerular disease?

A
  1. Reduce intraglomerular pressure
    a. Reduces proteinuria
    b. Delays onset of renal failure
178
Q

Why do thromboembolic events occur in glomerular disease?

A
  1. Believed to be secondary to ATIII loss
  2. More likely to occur if albumin < 2
  3. PTE is most common
179
Q

What is the most common form of glomerular disease in the cat?

A

Membranous nephropathy → second most common in dogs

  • Typically idiopathic
  • Immune complex deposition on the sub epithelial glomerular basement membrane and podocyte (urine)
180
Q

Proteinuria and nephrotic syndrome status in membranous nephropathy

A
  1. Proteinuria → severe

2. Nephrotic syndrome → common

181
Q

How is membranous nephropathy treated?

A

Immune suppression

  1. Chlorambucil and prednisone
  2. Cyclosporine
182
Q

What is the prognosis for membranous nephritis?

A

Cats: 50% euthanized for nephrotic syndrome and renal failure.

  • 20% short term survival (7 months)
  • 30% long term survival (>2 years)

Data similar in dogs

183
Q

What is the cause of amyloidosis?

A
  1. Deposition of A in β pleated form in the glomerulus
  2. Reactive amyloidosis is the most common form → 40% develop secondary to infectious, inflammatory, or neoplastic causes
184
Q

Proteinuria and nephrotic syndrome status in amyloidosis

A
  1. Proteinuria → severe

2. Nephrotic syndrome → common

185
Q

How is amyloidosis treated?

A
  1. Colchicine
  2. May help reduce development of renal amyloidosis but wont reverse it
  3. Decreases serum amyloid A from the liver
186
Q

What is glomerulosclerosis?

A
  1. End stage changes resulting from early glomerulonephritis

2. Glomerular membrane is too thick to function

187
Q

What CFU counts would be indicative of infection for the following collection methods?

  1. Cysto
  2. Catheter
  3. Free Catch
A
  1. > 1,000
  2. > 1,000 (cat), >10,000 (dog)
  3. > 10,000 (cat), >100,000 (dog)
188
Q

What is the prognosis for amyloidosis?

A

Poor

*Only 8% survive >1 year

189
Q

What are the antibiotics of choice for empiric UTI treatment?

A
  1. Amoxicillin

2. TMS

190
Q

What is the most common causative agent for fungal UTI? How is it treated?

A
  1. Candida
    - Aspergillus and cryptococcus are also possible
  2. Fluconazole

ACVIM General Old Questions 2 (15 decks)

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