Renal/Urinary Flashcards

1
Q

Vascular organization of the kidneys

A

Renal artery, segmental artery, interlobar artery, arcuate artery, radial artery, afferent artery, efferent artery, peritubular capillaries/vasa-recta, arcuate veins, interlobar veins, segmental veins, renal vein

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2
Q

Does the medulla contain glomeruli?

A

No the deepest glomeruli are at the junction bet

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3
Q

What are the three main cell types in the glomerulus?

A
  • endothelial cells
  • podocytes
  • mesangial cells
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4
Q

Kidneys receive ____ % of the CO, but only ____ % reaches the inner medulla

A
  • 20%
  • 5%

This is why the medulla is more prone to develop ischemic injuries

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5
Q

Are there glomeruli in the medulla?

A

No, the deepest glomeruli are found at the junction between cortex and medulla –> juxtaglomerular nephrones

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6
Q

Describe the two different capillary systems present in the kidneys

A
  • high pressure system –> glomerular capillaries
  • low pressure system –> peritubular capilaries
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7
Q

The efferent arteriole can progress into ____ if in cortical nephrones or into ____ if in juxaglomerular nephrones

A

a. peritubular capillaries
b. vasa recta

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8
Q

What is the renal threshold for glucose in dogs and cats?

A

Dog: 10-12 mmol/L
Cat: 15-18 mmol/L

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9
Q

Name glucose transporters in PT

A
  • luminal side
    SGLT-2 (proxymal - 1 glucose with 1 sodium)
    SGLT-1(distal - 1 glucose with 2 sodium)
  • basolateral
    GLUT transporter
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10
Q

What are the two main causes of hypocalcemia in dogs/cats with CKD?

A

1) hyperphosphatemia
2) Calcitriol deficiency

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11
Q

Where is renin release?

A

Juxtaglomerular cells

Granular cells?

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12
Q

Draw and label the juxtaglomerular apparatus. What are the three major components of juxtaglomerular apparatus?

A

1) Macula densa
2) Juxtaglomerular cells
3) Extra-glomerular mesangial cells

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13
Q

In the kidney, where does ammoniagenesis mainly happen? Which amino acid is the source?

A

Proximal renal tubule
Glutamine (NH4+ + HCO3-)

at physiological pH NH4 will never release H+ (excellent way to trap H+

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14
Q

Where is NH4+ reabsorbed? by which transporter?

A

Reabsorbed by the thick acending loop of Henle by NCCK transporter (using the K+ site).
Contributes to hyperosmolarity of medulla

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15
Q

True or False: Proteinuria is a negative prognostic indicator in both canine and feline CKD.

A

True

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16
Q

What is the flow in the hemodialysis filter that can optimize the dialysis efficiency?

A

Countercurrent flow

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17
Q

What are the four mechanisms of extracorporeal therapy?

A

Diffusion
Convection
Absorption
Ultrafiltration
Separation

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18
Q

What is the diffusion based on to make the particles move?

A

Concentration gradient
Membrane charististics

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19
Q

What is the mechanism behind convection in extracorporeal therapy?

A

Solvent drag
* Hydrostatic pressure gradient

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20
Q

What are the four factors to consider when you determine the modality of the extracorporeal therapy?

A

Protein-binding
Molecular weight
Volume of distribution
Patient’s volume status

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21
Q

What are the follow extracorporeal therapies based on?
Intermittent hemodialysis (IHD)
Hemoperfusion (HP)
Continuous venovenous hemofiltration (CVVH)
Continuous venovenous hemodialysis (CVVHD)
Continuous venovenous hemodiafiltration (CVVHDF)
Slow continuous ultrafiltration (SCUF)

A

Intermittent hemodialysis (IHD) - diffusion (+ultrafiltration but limited by short time)
Hemoperfusion (HP) - absorption
Continuous venovenous hemofiltration (CVVH) - convection
Continuous venovenous hemodialysis (CVVHD) - diffusion
Continuous venovenous hemodiafiltration (CVVHDF) - convection + diffusion
Slow continuous ultrafiltration (SCUF) - ultrafiltration
Therapeutic plasma exchange (TPE) - separation

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22
Q

True or False: Smaller molecules are better removed by diffusion, and larger molecules are better removed by convection.

A

True
* diffusion <500Da
* convection 500-60K Da

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23
Q

What is a safe rate of fluid removal via ultrafiltration

A

10ml/kg/h
Monitor CV stability (drop of SvO2)

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24
Q

Where should the tip of the dialysis cather lie? what flow rates should it allow for?

A

In the right atrium
Flow rates up to 150ml/min in cats and 500 ml/min in dogs

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25
Q

The port to the circuit should be proximal vs the port to the patient should be distal

A

True

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26
Q

Type of dialysis catheters

A
  • temporary
  • permanent
    surgically placed and tunnelled with cuff
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27
Q

If BUN>200mg/dL a larger and more efficient dialyser is preferred

A

False: higher risk of dysequilibrium syndrome - a smaller dialyser is preferred (also less chance of clotting)

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28
Q

Ideally the hemodialyser + tubing volume should equate to ____ of the patient’s blood volume

A

<10%

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29
Q

URR

A

URR = Serum [urea] before tratment - serum [urea] after treatment / serum [urea] before treatment

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30
Q

TAC

A

Integrated exposure to uremic toxins overtime

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31
Q

Dialysis dose

A

Kt = Kd x Td

Kd = clearance of the dialyser for urea (volume of blood cleared of urea in 1 min)
Td = dialysis time

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32
Q

Physics principles behind peritoneal dialysis

A
  • diffusion
  • ultrafiltration (very little convection with ultrafiltration possibly responsible of albumin loss)
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33
Q

Three pores model

A

Three types of pores in the capillary walls, each with a different size and function:
* ultrasmall (<0.8nm) = AQP
* small (4-6nm) = responsible for the majority of the solute transport in PD
* large (20-40nm) = occasional endothelial clefts (albumin)

Expression of AQP enhanced with exposure to hyperosmolar solutions

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34
Q

PD catheter

A
  • percutaneous
  • surgical with tunnelling and dacron cuffs
    Best type is T-flute
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35
Q

TPE cathegories

A

According to evidence of efficacy
* I: myastenia gravis and hypergammaglobulinemia
* II: IMHA
* III: IMTP, Sepsis (cytokines)
* IV: no evidence/detrimental

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36
Q

Processing 1.5x plasma volume with TPE removes up to____ % of toxic substance

A

80%

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37
Q

Dialysis treatment intensity

A

If no pre-calculated graphs are available an empiric approach must be adopted
When initial BUN > 300mg/dL (110 mmol/L) the Qb should be limited to 1-1.5mL/Kg/min
If BUN 150-300mg/dL the Qb should be limited to 1.5-2mL/Kg/min
Once BUN<150 mg/dL the Qb can be increased up to 5mL/Kg/min
For small animals the machine might not be able to provide safely slow Qb so can introduce ‘bypass intervals’ in which the blood flow continues but the dialysate flow ceases

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38
Q

Na profiling

A

[Na] in the dialysate adjusted systematically during dialysis session to counteract solute disequilibrium and promote vascular filling (prevent hypovolaemia/hypotension)
Initially dialysate is hypernatraemic to promote shift of sodium into the blood and vascular filling to counteract loss of volume due to circuit priming, ultrafiltration and compensate for the greatest initial urea shift (maintain osmolarity)

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39
Q

In IHD the ____ flow predicts clearance vs in CRRT the ____ predicts clearance

A

blood flow
dialysate flow

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40
Q

In CVVHF pre-filter fluid replacement reduces risk of clotting but…

A

decreases efficiancy as blood is diluted when passing through the filter

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41
Q

True or False: During hemodialysis for ethylene glycol intoxication, only ethylene glycol is removed and the metabolites remains in the system.

A

False

Both ethylene glycol and its metabolites are removed

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42
Q

Which extracorporeal system needs a water treatment system for the dialysate proportioning?

A

IHD

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43
Q

What are two types of water loss?

A

Obligatory water loss: water needed to excrete the daily renal solute load

Free water loss: water excreted unaccompanied by solute under the control of antidiuretic hormone [ADH]

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44
Q

In dogs, how many percentage increase of osmolality will induce thirst?

A

1 - 3%

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45
Q

Which molecule can be filtered through the glomerulus more easily, the positively charged or negatively charged one?

A

Positively charged one

Because glomerulus is negatively charged

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46
Q

What is the size selectivity limit of glomerulus?

A

7-9 nm in diameter (nephrin forming slit diaphragm in podocyte layer)

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47
Q

Which layer contributes to the glomerulus charge selectivity?
1) Capillary endothelium
2) Glomerular basement membrane
3) Visceral epithelial cells (podocytes)

A

2) glomerular basement membrane

The lamina rara interna and lamina rara externa contain polar non-collagenous proteins that contribute to the negative charge of the filtration barrier.

The lamina densa contains nonpolar collagenous proteins that contribute primarily to the size selectivity of the filtration barrier.

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48
Q

The glomerulus has similar net filtration pressure than systemic capillary, but why glomerulus has such high filtration rate than capillary?

A

1) The glomerulus has much bigger surface area for filtration
2) The permeability for electrolytes are much greater (100x) than systemic capillaries

Both contribute to higher ultrafiltration coefficient Kf

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49
Q

What are the changes in renal blood flow and GFR in each situation?

A
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50
Q

What are the effects of norepinephrine, angiotensin II and dopamine and ADH on the renal blood flow and GFR?

A
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51
Q

True or False: norepinephrine, angiotensin II and ADH cause renal arterioles vasoconstriction, and stimulate the production of (PGE2 and PGI2), which counterbalances by their vasodilation effect.

A

True

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52
Q

True of False: ADH causes vasoconstriction on both afferent and efferent arterioles, and prostaglandin E2 cause vasodilation on both afferent and efferent arterioles.

A

False

ADH only cause vasoconstriction on efferent arterioles; prostaglandin E2 only cause vasodilation on afferent arterioles.

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53
Q

What is the equation for GFR?

A
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54
Q

What is normal GFR for dogs and cats? What about renal plasma flow (RPF) and filtration fraction (FF)?

A

1) GFR: Dog 3-5 ml/kg/min Cat 2.5-3.5 ml/kg/min
2) RPF: Dog 7-20 ml/kg/min Cat 8-22 ml/kg/min
3)FF: Dog 0.32-0.36 Cat 0.33-0.41( approx 30%)

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55
Q

Name two substances that can used to evaluate GFR.

A

Creatinine
Inulin (a polymer of fructose)

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56
Q

Fill out the blank: In the kidneys, between perfusion pressures (MAP) of __________, GFR and RBF vary less than 10%. The ________ is the site to regulate the pressure.

A

80 - 180 mmHg

Afferent arterioles

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57
Q

What are the two autoregulation of nephrons? Which one is faster?

A

Myogenic mechanism
Tubuloglomerular feedback

Myogenic mechanism is faster

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58
Q

What is the RBF when compared to total cardiac output?

A

20% of cardiac output

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59
Q

How do you assess RBF based on RPF?

A
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60
Q

Which route does water mainly pass through in the renal tubule, paracellular route or transcellular route?

A

Transcellular route

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61
Q

Name four renal transport processes and an example for each one of them.

A

Passive diffusion -
Facilitated diffusion - glucose, amino acid
* it is a saturated process
Primary active transport - H+-ATPase at the luminal side, Na,K-ATPase at the basolateral side
Secondary active transport - (e.g. glucose-Na, Na-H)

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62
Q

True or False: Na is reabsorbed with glucose, amino acids, phosphate, and bicarbonate in the proximal renal tubule.

A

True

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63
Q

Which tubular transport maximum (Tmax) is the lowest, glucose, phosphate or amino acid?

A

Phosphate

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64
Q

Explain why during dehydration, patient’s BUN may increase but not creatinine?

A

50% or urea is passively reabsorbed in the proximal renal tubule. When patient is dehydrated, tubular flow decreases, there is increased water reabsorption and subsequent urea reabsorption via the solvent drag.
On the other hand creatinine is not reabsorbed and only increases after a significant drop in GFR.

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65
Q

True or False: The ascending limb of Henle’s loop is impermeable to water.

A

True

So NKCC2 can transport the electrolytes without carrying water → important step for urinary concentrating mechanism

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66
Q

There are three segments of collecting ducts, what are they? Which segment is permeable to urea?

A

Cortical, outer medullary, inner medullary

Inner medullar collecting duct is permeable to urea
* its urea permeability is increased by ADH

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67
Q

Why under normal condition, the medullary interstitium can maintain its hyperosmotic gradient?

A

The countercurrent exchange of vasa recta → can remove water while keep the solutes in the interstitium

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68
Q

Explain countercurrent mechanism

A
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69
Q

Where is erythropoietin EPO produced in the fetus and adults?

A

Fetus: liver
Adults: peritubular cells in kidneys

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70
Q

Name three conditions that will increase renin release.

A

1) Decreased renal perfusion pressure (release of PGI2 from endothelium and stimulation of granular cells)
2) SNS stimulation & increased circulating catecholamines level (𝛽1 receptors on granular cells)
3) Decreased Cl concentration at the distal tubular flow (release PGE2 by macula densa cells and stimulation granular cells)

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71
Q

In the RAAS system, which step is the rate limiting step?

A

Renin converts 𝜶2-globulin angiotensinogen to angiotensin I

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72
Q

True or False: The release of renin is inhibited by a direct effect of angiotensin II on the granular cells.

A

True

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73
Q

How does angiotensin II cause increase proximal renal tubular sodium absorption?

A

Stimulating the Na-H antiporter in luminal membranes of proximal tubular cells.

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74
Q

Name 5 functions of angiotensin II

A

1) arterial vasoconstriction
2) inhibit renin
3) stimulate aldosterone production
4) stimulate ADH release
5) stimulate mesangial cells to produce PGE2, PGI2
6) Increase proximal renal tubular Na reabsorption
7) Cause afferent and efferent renal arterioles constriction

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75
Q

Where in the kidney is calcidiol converted to calcitriol?

A

Proximal tubular cells

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76
Q

Name 5 different types of diuretics, which part of the renal tubules do they work on and their MOA.

A

1) Carbonic anhydrase inhibitor - acetazolamide
2) Osmotic diuretic - mannitol
3) NKCC2 inhibitor - furosamide, torsamide
4) Thiazide - thiazide
5) Aldosterone receptor antagonist - spironolactone

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77
Q

Mechanism of action of Vaptans

A

ADH receptor antagonists
Also called aquaretics

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78
Q

Mechanism of action of venagliflozin (Senvelgo)

A

SLG-2 inhibitor –> osmotic diuresis due to impaired glucose reabsorbtion
in dogs increased urine volume by 3.7x and natriuresis by 1.5x
Consider in cases of diuretic resistance

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79
Q

Why do thiazide diuretic cause hypercalcaemia?

A

By blocking Na/Cl they induce a lower intracellular [Na+] which causes hyperactivity of the Na/Ca exchanger on the basolateral membrane –> increased gradient for Ca++ reabsorbtion

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80
Q

Mechanism of action of xanthines

A
  1. increased CO = increased GFR
  2. A1 receptor antagonists = reduced NH3 activity in PT
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81
Q

What is MOA of Acetazolamide?

A
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82
Q

According to IRIS CKD staging, what is the UPC cutoff for proteinuria in dogs and cats? What about the cutoff for pre-hypertensive and hypertensive?

A

UPC
Dog: > 0.5
Cat: > 0.4

Blood pressure
Pre-hypertensive 140-159
Hypertensive 160-179

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83
Q

What is the creatinine range for grade II AKI?

A

140-220 umol/L

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84
Q

According to IRIS AKI grading system, what is the definition of fluid responsive?

A

UOP > 1 ml/kg/hr over 6 hours, or creatinine decrease to baseline over 48 hours

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85
Q

What are the two subgrading for AKI in IRIS guidelines?

A

1) Non-oliguric or Oligo-anuric
2) Requiring RRT

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86
Q

According to IRIS AKI grading system, how many days does it normally take for grade I and II AKI to regain adequate renal function?

A

2-5 days

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87
Q

What are the three mechanisms of pathological causes of diuresis?

A

1) Failure of ADH to function
2) Pressure diuresis (e.g. hypertensive hypervolemic state)
3) Osmotic diuresis (e.g. glucosuria)

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88
Q

Among all classes of diuretics, which one reach its site of action from the blood instead of urinary space?

A

Spironolactone

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89
Q

How does furosemide reach its site of action?

A

Not freely filtered as highly protein bound, so via blood to the baso-lateral membrane where picked up by OAT (competition with NSAIDs and uremic anions) transporter and then excreted to lumen by MRP4

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90
Q

What is the MOA of amiloride?

A

Amiloride is not an aldosterone receptor antagonist like spironolactone, but a direct inhibitor of ENaC → excrete water, retain K and H+

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91
Q

What is the MOA of acetazolamide?

A

Inhibits type II (cytoplasmic) and type IV (membrane) carbonic anhydrase at the proximal renal tubule → decrease reabsorption of sodium bicarbonate

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92
Q

How many percentage of Na is reabsorbed at the proximal renal tubule, loop of Henle, distal convoluted tubule and collecting duct, respectively?

A

Proximal renal tubule: 67% (2/3)
Loop of Henle: 25%
Distal convoluted tubule: 5%
Collecting duct: 3%

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93
Q

What are 4 types of renal tubular acidosis?

A

Type I (classic distal RTA): inability of distal renal tubule to excrete H+
- Hyperchloremic metabolic acidosis + increased urine pH (pH > 6.0)
- Ammonium chloride challenge test

Type II (proximal RTA): inability of proximal renal tubule to prevent loss of bicarbonate
- Mild metabolic acidosis + acidic urine or alkalotic urine (bicarbonate can be reabsorbed in the distal tubule as long as the concentration is <20mEq, if more bicarbonate is lost in urine)
- HCO3- fraction excretion > 15% after normalizing the plasma bicarbonate (normally is < 5%)

Type IV (hyperkalemic distal RTA): distal RTA and hyperkalemia secondary to hypoaldosteronism or aldosterone deficiency

Type III: a rare combination of proximal and distal RTA caused by carbonic anhydrase II deficiency and carbonic anhydrase inhibitors blocking the metabolism of bicarbonate and carbonic acid

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94
Q

List 5 lab abnormalities of Fanconi syndrome. Which segment is affected?

A

1) Proximal renal tubular acidosis (normal AG hyperchloremic acidosis)
2) Glucosuria, proteinuria, aminoaciduria, phosphaturia, hypophosphatemia.

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95
Q

Nephrotoxic mechanisms of aminoglycosides

A
  • membrane accumulation in tubular epithelium due to positive chages attracted by negative phospholipid layer (neomycin most toxic due to most positively charged)
  • lisosomal accumulation when internalised
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96
Q

How many percentage of calcium is reabsorbed at the proximal renal tubule, loop of Henle, distal convoluted tubule and collecting duct, respectively?

A

Proximal renal tubule: 60-70% (paracellular)
Loop of Henle: 20% (paracellular)
Distal convoluted tubule: 10% (transcellular)
Collecting duct: almost none

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97
Q

The release of vasopressin is more sensitive to change in osmolarity or effective circulating volume?

A

osmolarity

An increase of only 1% in plasma osmolality will stimulate vasopressin release, whereas a drop in blood volume of approximately 10% is needed to stimulate vasopressin release

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98
Q

List 8 causes of Nephrogenic diabetic Insipidus (NDI).

A

Hypercalcemia
Hypokalemia
Pyelonephritis
Pyometra or gram (-) sepsis
Hyperthyroidism
Hypoadrenorcorticism (decreased Na → unable to maintain the interstitial concentration gradient)
Hepatic insufficiency (decreased urea production → unable to maintain the interstitial concentration gradient)
PSS (decreased urea production → unable to maintain the interstitial concentration gradient)

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99
Q

When performing desmopressin acetate trial, what is your interpretation if urine concentration does not change and remain hyposthesuria?

A

NDI or psychogenic polydipsia

100
Q

What is the proposed mechanism of pulmonary disease causing SIADH?

A

1) tumors that ectopically produce ADH
2) diseases that interrupt the inhibitory impulses in vagal afferents from stretch receptors in the atria and great veins

101
Q

What is the most significant clinical signs of SIADH?

A

Clinical signs associated with hyponatremia

  • NO hypertension or edema will be present
  • An increased BUN concentration typically excludes a diagnosis of SIADH
102
Q

Name 3 novel urinary biomarker for glomerular injury and 3 for renal tubular injury.

A

Glomerular injury: urine CRP, urine IgG, albuminuria

Tubular injury: urine GGT & ALP (proximal renal tubule brush border), NGAL (multiple tissue, reabsorbed at proximal renal tubules), cystatin B (ruptured proximal renal tubule epithelial cells), clusterin and KIM-1 (damaged PT)

GFR
cystatin C (most nucleus cells)

103
Q

What are the 4 phases of acute renal injury?

A

Insult: first renal injury
Initiation: cellular damage
Extension: cellular death
Maintenance: balance between cellular death and regeneration
Recovery: regeneration vs fibrosis

104
Q

What are the most common lesions for CKD in dogs and cats, respectively?

A

Dog: glomerular disease/interstitial nephritis
Cat: lymphoplasmacytic tubulointerstitial nephritis

105
Q

Fill in the blank: Typically, dogs with a urine protein-to-creatinine ratio of at least ____ are likely to have glomerular disease.

A

2

106
Q

List 5 things that are associated with mortality in cats with CKD.

A

Plasma creatinine concentration
UPC
Urine albumin-to-creatinine ratio
Leukocytosis
Hyperphosphatemia

107
Q

Fill out the blank: A urine sodium level of__________ is consistent with the action of aldosterone and supports the presence of poor renal perfusion.

A

less than 20 mEq/L

108
Q

Fill out the blank: A urine sodium level of _________ with concurrent hyponatremia supports the diagnosis of SIADH.

A

more than 40 mEq/L

109
Q

Name 3 contraindication for hemodialysis and peritoneal dialysis.

A

Hemodialysis: severe coagulopathy, severe hemodynamic instability, small patient size

Peritoneal dialysis: recent abdominal surgery, hypoalbuminemia, peritonitis

110
Q

What is the definition of catheter-associated bacteriuria? What about catheter-associated UTI?

A

Catheter-associated bacteriuria
1) urine sample obtained aseptically from the urinary catheter or within 48 hours after urinary catheter removal
2) test positive for 1 species of bacteria at 10^5 CFU/ml

Catheter-associated UTI
1) Fever or clinical signs associated with UTI
2) test positive for 1 species of bacteria at 10^3 CFU/ml

111
Q

What is the outer diameter of a 12 Fr urinary catheter?

A

4 mm

French scale = external diameter x 3

112
Q

What is the MOA of fenoldopam?

A

D1 dopamine receptor agonist → cause vasodilation, especially at the renal capillary bed → increase renal blood flow

113
Q

What is the MOA of diltiazem in treating oliguria?

A

Calcium channel blocker → cause afferent arteriole vasodilation → increase GFR

114
Q

True or False: UTIs in intact male dogs are classified as complicated infections.

A

True

Because prostatic disease is commonly involved

115
Q

What bacteria can facilitate struvite urolith formation when they present in the urine (name 3).

A

Staphylococcus spp
Proteus spp
Corynebacterium spp

Due to alkalinization of urine by urea metabolism by these organisms (urease)

116
Q

True or False: Urine pH is often alkalotic with E. coli infections.

A

False

Acidic

117
Q

What is the most common bacteria for acute prostatitis

A

E. coli

118
Q

Name 3 uroliths that exist in acidic urine

A

Calcium oxalate
Purine
Cystine

119
Q

Name two uroliths that are considered non-radiopaque.

A

Urate
Cystine

120
Q

What is the full name for struvites

A

Magnesium ammonium phosphate hexahydrate

121
Q

Which urolith cannot be dissolved by diet?
1) struvites
2) calcium oxalate
3) cystine
4) xanthine

A

calcium oxalate

122
Q

What are the two important factors that promotes urethral healing?

A

1) Prevent urine extravasation
2) Good mucosal continuity

123
Q

How long does it take for urethral mucosa to regenerate?

A

7 days

124
Q

In male dogs and male cats, what are the urethrostomy recommended?

A

Male dog: scrotal urethrostomy
Male cat: perineal urethrostomy

125
Q

How to differential hemoglobinuria from myoglobinuria with ammonium sulfate test?

A

80% ammonium sulfate solution is added to a urine sample and the mixture is observed for precipitation of the colored substance

Soluble → myoglobinuria
Insoluble → hemoglobinuria

126
Q

What is the landmark on palpation when you place a urinary catheter in female dogs?

A

Urethral papilla

127
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the cut-off frequency for sporadic cystitis and recurrent cystitis?

A

Sporadic: < 3 eposides in 12 months
Recurrent: ≥ 3 episodes in 12 mouths

  • A single recurrence of sporadic cystitis within the preceding 3 months should be approached recurrent cystitis
128
Q

True or False: According to the ISCAID guidelines for the bacterial UTI in dogs and cats, NSAIDs are contraindicated in patients with sporadic cystitis as they can worsen the clinical signs.

A

False

NSAIDs (use with caution in cats) should be considered during the initial treatment period to help ameliorate clinical signs.

129
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the recommended first-line antibiotic and treatment duration?

A

Amoxicillin
3-5 days

130
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, post-treatment urine culture should be performed in sporadic cystitis 48 hours after the treatment is finished.

A

False

Post-treatment urinalysis or urine culture is NOT recommended for sporadic cystitis when clinical signs have resolved.

131
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the recommended duration of treatment for recurrent cystitis?

A

Re-infection:3-5 days

Persistent: 7-14 days

132
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, how to approach recurrent cystitis?

A

Investigations for co-morbidities: imaging, cystoscopy, urine C&S +/- bladder biopsies.

While waiting for C&S start empiric treatment with same antibiotic as last time.
If different bacteria isolated then treat as simple infection with 3-5 days abx treatment and if clinically improved → no culture needed

If same previous bacteria isolated 7-14 days treatment → can consider culture after 5-7 days of treatment but mandatory to repeat culture 5-7 days after the treatment is finished

133
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the recommended first-line treatment and duration of treatment for pyelonephritis? When to recheck (urine culture)?

A

Fluroquinolone or cefpodoxime (3rd generation antibiotic)

10-14 days

1-2 weeks after the treatment is finished

  • Consider serum breakpoint instead of urine breakpoint!
134
Q

Antibiotic with what characteristic is most likely to cross the prostate-blood barrier (e.g. lipophilic vs hydrophilic, pKa, acidic & alkaline)?

A

Lipophilic, weak alkaline, high pKa

135
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the target organism for bacterial prostatitis before the culture result returns?

A

Enterobacteriaceae

136
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the recommended antibiotics for bacterial prostatitis before the culture result returns and the duration of treatment?

A

Fluoroquinolone, TMS
4-6 weeks

137
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the definition of subclinical bacteriuria?

A

Positive culture of bacteria in the cystocentesis urine WITHOUT clinical signs

  • NOT based on urine sediment or cytology!
138
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the cut-off of CFU/ml to differentiate sporadic cystitis from subclinical bacteriuria?

A

You CAN’T differentiate them with bacterial cell count

139
Q

True or False: Treatment of animals with pyuria or other cytological abnormalities without lower urinary tract signs is not recommended.

A

True

140
Q

True or False: According to the ISCAID guidelines for the bacterial UTI in dogs and cats, routine catheter replacement to prevent bacteriuria or cystitis is not recommended.

A

True

141
Q

True or False: According to the ISCAID guidelines for the bacterial UTI in dogs and cats, routine cytological evaluation and urine culture in patients with an indwelling urinary catheter is recommended to screen for UTI.

A

False

Unless there are clinical signs

142
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what should you do if a patient with an indwelling urinary catheter who develops signs of bacterial cystitis, but still requires the indwelling catheter in place?

A

1) Remove the urinary catheter
2) Collect urine by cystocentesis
3) Replace a new urinary catheter
4) After the clinical signs resolve with treatment, replace a new urinary catheter

  • After clinically-apparent resolution of catheter-associated bacterial cystitis, if the catheter cannot be removed, it should be replaced with a new catheter, since colonization of the catheter is likely, even with clinically successful treatment.
  • If this is not possible, the catheter should be removed, a new catheter placed and urine collected from the new catheter for culture. The !rst 3–5 mL of urine collected should be discarded before collecting the urine specimen for culture.
143
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, what is the recommendation for pre-operative screening for those patients that require urological surgery?

A

1) Urine culture to detect bacteriuria
2) If signicant bacteriuria is identified, treatment based on susceptibility result is indicated for 3–5 days duration immediately before the procedure

144
Q

According to the ISCAID guidelines for the bacterial UTI in dogs and cats, if antibiotic is indicated in patients who receive medical treatment to dissolve uroliths, how long the duration of treatment should be?

A

7 days

  • If bacterial cystitis is identified, antibiotic is recommended
  • If a urease-producing bacterium (e.g. Staphylococcus pseudintermedius,Proteus spp.) is identified, antimicrobials should be administered
145
Q

Formulas for:
* Clearance
* Fractional clearance
* Fractional excretion

A
  • Clearance = Urine [x] x Volume urine / Plasma [x]
  • Fractional clearance = Clearance[x] / Clearance [crea]
  • Fractional excretion = U[x] x P[crea]/ P[x] x U[crea]
146
Q

In human nephrology, what dose RIFLE stands for?

A

Risk
Injury
Failure
Loss of renal function
End-stage kidney disease

147
Q

Difference between RIFLE and AKIN

A

RIFLE relies on GFR (or crea) and UOP
AKIN relies on crea value and UOP but in the stage I there is a new concept of crea increase of 0.3mg/dl (26umol/L) being significant even if not 1.5x crea baseline
AKIN therefore is more sensitive and highlight an improtant redflag in hospitalised patients (discontinue nephrotoxic drugs, investigate UTI or pyelonephritis)

148
Q

KIDGO

A

Merging RIFLE and AKIN including need of RRT in stage III

149
Q

VAKI

A

AKIN for small animals
Mortality for stage 0 is <15% vs up to 54% in stage 1-3

150
Q

Define IRIS AKI stage I, II and III

A

IRIS classification based on crea value and clinical description
* stage I (non-azotemic aki): crea <140 umol/L, with oliguria or an increase of >26umol/L in 48h
* stage II (mild AKI): crea between 140-220 umol/L
* stage III-V (moderate to severe AKI): 220-440, 440-880, >880 umol/L

Additionally each stage is classified as”
* oliguric vs non-oliguric
* RRT dependent vs non-RRT dependent

151
Q

What is the relationship between RIFLE stage and mortality risk?

A

“Risk” cathegory mortality odd ratio of 1.58
“Injury” 2.54
“Failure” 3.22

152
Q

What is SDMA?

A

Symmetric dimethylarginine

It is produced by post‐translational methylation of arginine residues in proteins.
Two metabolites formed ADMA and SDMA. ADMA metabolised via enzymatic route vs SDMA 90% excreted and non-reabsorbed via renal route. Highly associated with GFR, not influenced by muscle mass (vs crea) and earlier indicator of decreased GFR.

153
Q

What are 5 phenotypes of cardiorenal syndrome (human medicine)?

A

Type I: acute cardiorenal syndrome
Type II: chronic cardiorenal syndrome
Type III: acute renocardial syndrome
Type IV: chronic renocardial syndrome
Type V: secondary cardiorenal syndrome

154
Q

How to measure RPF?

A

Measure a plasma marker that completely disappers from circulation after passing the glomerulus: Para-amino hippuric acid (PAH) CRI

RPF = (U PAH x Volume urine) / Plasma PAH

155
Q

Filtered load

A

amount of substance filtered into the Bowman’s space per unit of time
FL (mg/ml/min) = GFR x Plasma [x]

Take into consideration protein-binding!!

156
Q

What is the filtered load of Ca++ with a Tcal of 0.095mg/mL and a GFR of 125ml/min?

A

Ca++ bound to protein is 40% –> only 60% Tcal is actually filtered –> (0.095/100)x60 = 0.057 mg/mL

FL = GFR x [ free Ca] = 125 x 0.057 = 7 mg/ml/min

157
Q

What is the equation to calculate fractional excretion of sodium?

A

Hemodynamic instability causing azotemia: FEna < 1%

Intrinsic renal damage causing azotemia: FEna > 1%

  • When aldosterone is secreted, the kidneys can conserve sodium such that in hypovolemic states, the urine Na+ should be <20 mEq/L and may be as low as 1 mEq/L.5 Values of 20-40 mEq/L are equivocal, while >40 mEq/L of Na+ implies the kidneys are interpreting a normal blood volume
158
Q

Fractional excretion of Na is a prognostic indicator in dogs with AKI

A

True: improvements in FE (decrease) of Na during hospitalisation reliably forecasted renal recovery and it occurred prior to azotemia resolution or dialysis independence

159
Q

Why is fractional excretion preferred to clearance in the clinical settings? Are they significantly correlated?

A

FE only requires spot measurements vs Clearance requires U cath and collection urine over time.
Studies have shown reliable correlation between the two values.

160
Q

Describe percutaneous nephrostomy tube placement (using locking-loop pigtail nephrostomy catheters)

A

Each patient was placed in lateral recumbency with the affected kidney in the up position. Antimicrobials (cefazolin) were given (22 mg/kg [10 mg/lb], IV, at induction and q 2 h during the procedure) if patients were not currently being treated with antimicrobials. The area over the kidney was clipped of hair and aseptically prepared. A small stab incision was made in the skin for catheter penetration.

Modified Seldinger technique Ultrasound guidance was used to perform pyelocentesis with an over-the-needle standard IV catheter or renal access needlec (dog, 18 gauge; cat, 22 gauge). Once the tip of the catheter was in the renal pelvis, the stylette was removed and an extension set and 3-way stopcock were attached to the catheter. Urine was drained and an equal amount of diluted contrast solutiond (50% contrast: 50% sterile saline [0.9% NaCl]) was infused into the renal pelvis to perform a pyelogram. Urine was submitted for microbial culture and antimicrobial susceptibility profiling. Under fluoroscopic guidance, an angle-tipped hydrophilic guidewire (dog, 0.035-inch-diameter wire; cat, 0.018-inch-diameter wire) was advanced through the catheter and coiled inside the renal pelvis. The catheter was removed over the wire, and the PNC (cat, 5Fg; dog, 6Fh) was advanced through the skin, into the renal parenchyma, and into the renal pelvis. Once the tip of the PNC was inside the renal pelvis, the cannula was immobilized as the catheter was advanced over the guidewire to form its loop. Once the loop of the pigtail was completely within the renal pelvis, the loop of the catheter was locked in place by pulling on the locking string at the catheter hub (Figures 1 and 2) and the string was carefully locked and secured. The cannula was removed from the catheter. The catheter was secured to the body wall by means of a purse-string and Chinese finger trap suture pattern and a second butterfly suture along the shaft of the catheter to the body wall. A sterile urine collection system was attached to the catheter for gravity drainage. A secure abdominal bandage was placed.

Reference:
2012 JAVMA Use of locking-loop pigtail nephrostomy catheters in dogs and cats: 20 cases (2004–2009)

161
Q

What is the normal diameter of feline ureter?

A

0.4 mm

162
Q

What sympathetic nerve and adrenergic receptor are in charge of the bladder function? What happen when it is activated?

A

Hypogastric nerve (leave the spinal cord at TS region)

Detrusor muscle relaxation (𝜷 receptor)
Urethral smooth muscle contraction (𝜶 receptor)
→ urine retention

163
Q

What parasympathetic nerve and somatic nerve are in charge of the bladder function? Where do they originate from? What happen when they are activated?

A

Parasympathetic nerve - pelvic nerve
- Detrusor muscle contraction (M3)
- Inhibit sympathetic and pudendal nerve (from micturition center in pons)

Somatic nerve - pudendal nerve
- Striated urethral muscle contraction (N1 nicotinic - striated muscle)

S1-S3

164
Q

How to close the cystotomy bladder?

A

Single layer, continuous or intermittent appositional pattern with monofilament absorbable suture

165
Q

What is the MOA of Phenylpropanolamine (PPA; Proin)? What is the indication?

A

Cause release of NE and decrease the reuptake
𝜶1 agonist (mainly)
𝜷 agonist (weak)

Treat urethral sphincter hypotonus (or hormone responsive incontinence)
* Often in spayed female due to decrease estrogen
* Dose: 2 mg/kg BID

166
Q

What is the MOA of bethanechol? What is the indication?

A

Cholinergic muscarinic receptor agonist (M3).
It doesn’t affect nicotinic receptors of the external sphincter.

Lower motor neuron bladder, detrusor muscle atony
Dose: 2.5 - 25 mg/dog BID-TID

167
Q

Explain the pathophysiology of detrusor muscle atony.

A
  • Injury to the sacral spinal cord S1 - S3 or pelvic nerves (impaired parasympathetic tone)
  • Direct damage to the detrusor muscle (e.g. overdistension caused by mechanical or functional outflow obstruction of an acute or chronic nature). The muscle fibers of the detrusor transmit action potentials that initiate contraction via tight junctions. With overdistension, these tight junctions are interrupted, leading to an absent or ineffective contraction.
168
Q

What is MOA of tamsulosin?

A

𝜶1A antagonist

𝜶1A receptors are specific of prostate and uretra vs 𝜶1B in vessels –> no hypotension vs prazosin
Also tamsulosin only to be administered q24h vs prazosin q8-12h

169
Q

What is the proposed pathophysiology of FIC?

A

Imbalance between the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis brought about by stressful situations
→ impaired blood flow & release of inflammatory mediators
→ edema, smooth muscle spasm, pain within the lower urinary tract

170
Q

List 4 possible pathophysiology of post-obstructive diuresis (POD).

A

1) Medullary washout
2) Accumulation of osmotically active substances in the blood (osmotic diuresis)
3) Renal tubular damage/dysfunction
5) Increases in natriuretic factors brought about during the obstructive process

171
Q

What are the pros and cons of each of the following urinary catheter:
Polypropylene
Polyvinyl
Polytetrafluoroethylene
Polyurethane

A

Polypropylene (Tomcat): most rigid, more reactive and irritating to tissue, more likely to cause urethral trauma
Polyvinyl (Red rubber): less rigid than tomcat, usually only comes with a side hole (not ideal for the initial un- blocking process), can be irritable
Polytetrafluoroethylene: firm at room temperature but soften when warmed to body temperature (meaning they can be left in place), less reactive to tissue
Polyurethane: firm at room temperature but soften when warmed to body temperature (meaning they can be left in place), cause least tissue reaction

172
Q

What types of muscles does feline urethra composed of? What about dogs?

A

Proximal 1/3: smooth muscle
The rest 2/3: skeletal muscle

Dogs:
Proximal 2/3: smooth muscle
The rest 1/3: skeletal muscle

173
Q

Which of the following mechanism is not used in peritoneal dialysis?
1) Diffusion
2) Convection
3) Ultrafiltration

A

2) Convection

174
Q

In peritoneal dialysis, what is the normal glucose concentration in dialysate? What if patient is overhydrated?

A

Normal: 1.5%

Overhydrated: 2.5% or 4.25%

  • Heparin (250– 1000 U/L) should be added to the dialysate for the first few days after catheter placement to help prevent occlusion of the catheter by fibrin deposition
175
Q

Describe how many mL of dialysate should be infused over how long? What is the indwelling time and drainage time?

A

Infusion volume: 20-40 ml/kg

Infusion time: 10-20 min

Indwelling time: 30-40 min

Drainage time: 10-20 min

Ideal retrieval percentage: 90-100%

176
Q

What is the important to do at the beginning of each infusion to prevent bacterial contamination/infection?

A

At the beginning of every exchange, 2 mL of dialysate should first be flushed through the stopcock and into the outflow bag.

This is referred to as the drain first protocol.

177
Q

List 5 complications of PD.

A

1) Hypothermia
2) Outflow obstruction
3) Hypokalemia
4) Hypoalbuminemia
5) Dialysate leakage

178
Q

What is the diagnostic criteria for peritonitis in patient with PD?

A

Meet at least 2 of the following criteria
1) Cloudy dialysate effluent
2) Detection of >100 inflammatory cells/𝜇L, or organisms in gram stain or cultures
3) Clinical signs of peritonitis

179
Q

What is nephrin? Why is it important?

A

Zip-like sturcture of the podocyte slit diaphragm
If missing no size selectivity - severe proteinuria occurs

180
Q

List the main mechanisms for GFR regulation

A

Intrinsic
* myogenic mechanism
* Tubulo-glomerular feedback
Extrinsic
* RAAS
* SNS
Others
* glucose –> arteriole vasodilation
* increased protein load –> production NO –> vasodilation afferent –> increased GFR
* endothelin –> vasoconstriction with drop of GFR

181
Q

Renal secretion of organic cations

A
182
Q

Renal secretion of anions

A
183
Q

Handling of urea

A

Urea is freely filtered, 50% reabsorbed in PT by passive diffusion (favorable gradient with interstitium). 50% is then secreted back into the lumen in the ascending loop of enle due to hyperosmotic medulla favoring secretion. Urea then gets recycled back into the interstitium at the level of the medullary collecting ducts

184
Q

Handling of urate

A

Constantly produced from protein metabolism.
In PT: 90% reabsorbed via OAT (URAT-1) and 10% secreted by K-butirrate recycling.

185
Q

How does urine pH influences secretion/reabsorbtion?

A
  • acid pH = weak acid not dissociated = more lipophilic = more passively reabsorbed
  • alkaline pH = weak basis not dissociated = more passively absorbed
186
Q

ADH also acts on the ascending loop of Henle

A

True: increases activity of NKCC pump = more re-absorbtion of Na and K

187
Q

Cellular mechanism of tubulo-glomerular feedback

A
  • increased delivery of ~Cl- in distal tubule sensed by macula densa cell via increased activity of NCCK. Increased intake of Na+ = swelling of the cell and increased activity of Na/K ATPase –> leakage of ADP and adenosine –> A1 receptors on afferent arteriole smooth muscle = Gi coupled –> vasoconstriction
  • decreased delivery of Cl- in the distal tubule –> decreased NCCK activity –> release of PGE2 –> receptor on granular cells –> production of renin + vasodilation of smooth muscle
188
Q

Myogenic mechanism

A

Stretch receptors are Na channel that open to depolarize smooth cell of afferent arteriole –> vasoconstriction

189
Q

Endocrine function of the kidneys

List 4 hormones produced by the kindeys

A
  1. EPO (by modified cortical fibroblest stimulate dby AGII and hypoxia, inhibited by inflammatory cytokines)
  2. Renin (granular cells in macula densa)
  3. Thrombopoietin (PT cells, stimulated by thrombocytopenia and inflammatory cytokines)
  4. Urodilatin (natriuretic peptide produced by distal and collecting tubules when sensing large amount of Na delivered –> paracrine messaging via c-GMP)
190
Q

List 5 hormones metabolised or cleared by the kidneys

A
  • activation of calcidiol in calcitriol in PT
  • insulin is freely filtered and completely reabsorbed in PT to be degraded by endosomes
  • gastrin (mechanism unknown)
  • vasopressin
  • oxytocin
  • PTH
  • TSH
  • GH
  • LH
191
Q

What is the rationale behind combination of hypertonic saline and furosemide to resolve refractory hypervolemia (i.e. CHF)

A
192
Q

Additional benefits of furosemide

A
  • reduced oxygen consumption (NCCK is ATP dependent pump)
  • by blocking NCCK pump it inhibits TG feedback –> vasodilation
193
Q

Torasemide vs furosemide

A

Tprasemide more potent, better oral bioavailability, suspected aldosterone antagonism activity

194
Q

According to a recent JVECC study contrast use is not associated with development of AKI in dogs

A

False: use of contrast has been shown to increase incidence of nephropaty in hospitalised dogs and the association was found to be dose- and type- dependent.
Overall incidence 7.6%.
Non-ionic iso-osmolar contrast safer.

195
Q

Mechanism of contrast medium nephrotoxicity

A
  • direct toxic damage to tubular cells
  • increase in endothelin and adenosine –> vasoconstriction
  • oxydative damage
196
Q
A
197
Q

Most common causes of AKI in dogs and cats

A

Dogs mainly secondary to systemic disease causing decreased renal perfusion (i.e. sepsis, sirs, DIC, liver failure, etc.) vs Cats pyelonephritis, ethylene glycol and lily’s tox

198
Q

What is the issue with the current available biomarkers? which would be the ideal ones? and which one are emerging now?

A

The current available ones are functional markers, the emerging ones are cellular damage markers, the ieal ones would be cell stress markers (i.e. metalloproteinase inhibitors and insulin-like growth factor binding protein)

199
Q

A BUN/Crea >20 is consistent with renal AKI

A

False: in renal AKI BUN/crea is <15 as intrinsic renal damage so BUN re-absorbtion impaired vs pre-renal and early obstructive AKI BUN absorbtion enhanced due to slow flow through tubuli and intact tubular cells

200
Q

Complications of azotaemia

A
  • Plt dysfunction (reduced receptor affinity for vWf)
  • pericarditis
  • encephalopathy and seizure
  • metabolic acidosis
  • risk of fluid overload
  • drug accumulation
  • hyperkalaemia
201
Q

Why is metoclopramide better avoided in the treatment of GI signs in AKI patients?

A

Metoclopramide mainly cleared by renal route vs ondansetron and maropitant mainly hepatic

202
Q

Treatment of hypertension in AKI patients

A

Incidence up to 80% in dogs and 60% cats and negatively associated with outcomes.
Main cause is usually a positive fluid balance, so first try to achieve a negative fluid balance. If still persisting consider amlodipine either PO or rectal

203
Q

Fluid de-escalation

A

once UOP, BUN and biochemical values stabilised, try to decrease IVFT rate by 25% daily while keep monitoring all parameters

204
Q

Definition of fluid overload

A

acute BW increase of 10%

205
Q

In the IRIS guidelines for diagnosis and management of AKI in dogs and cats dopamine is one of the recommended treatments

A

False: no evidence to improve GFR or outcome + increased HR and myocardial oxygen demand, reduce splancnic perfusion and decrease immune function

206
Q

Bicarbonate administration (pH<7.2) is associated with improved outcomes and increased number of RRT free-days in human patients with AKI

A

True
No evidence in SA, IRIS consensus states it is reasonable when:
* pH<7.2
* bicarb <16 mmol/L
* no respiratory acidosis
* all other causes of metabolic acidosis have been addressed

207
Q

How many patients with AKI have abnormal cPLi?

A

Up to 60%

208
Q

How many patients with AKI present with concurrent respiratory compromise?

A

up to 33%
* fluid overload
* Pulmonary haemorrhage with Lepto

209
Q

In AKI patients should be fed a protein restricted diet

A

False: ensure adequate amount of protein (not associated with worsening azotaemia and positively correlated with improved nitrogen balance) and easily digestible diet

210
Q

Adjusted interval drug dosing in AKI

A

New interval = (normal GFR/measured GFR) x normal dosing interval

In vet med no mean of accurately measure GFR in clinical settings

Estimated GFR according to IRIS grading:
* Grade III >50ml/min
* Grade IV 10-50 ml/min
* Grade V <10ml/min

Normal GFR > 100ml/min

211
Q

Prognosis in AKI

A

Reported mortality up to 34%
Hospital acquired AKI 9%

  • severity of azotaemia is not a good predictor of reversibility and recovery potential
  • lack of azotaemia improvement in the first few days of treatment is not a reliable indicator of possible recovery - 45% of patient with AKI discharged with increased renal values, but an additional 20% reached normal values in the subsequent months
  • animals with a past episode of AKI should be considered in stage I IRIS despite normal values and ongoing regular monitoring is recommended (first check within a week of discharge then every 3m for the first year)
212
Q

Prognostic indicators for AKI

A
  • IRIS stage
  • anuria
  • anaemia
  • thrombocytopenia
  • hypoalbuminaemia
  • metabolic acidosis
  • increased liver enzymes and Tbil
213
Q

Incidence of AKI in septic patients and pathophysiology

A

16%
* Abnormal RBF distribution (high flow with severe efferent vasodilation, but shunting of glomerulus) flow/filtration mismatch
* tubular damage by inflammatory mediators and ROS

214
Q

What is the main mechanism of nephrotoxicity for NSAIDs

A
  • inhibition of PGE2 during TG feedback mechanism
215
Q

Classification of micturition disorders

A
  • Neurogenic
  • UMN (pons-L7): hard inexpressible bladder
  • LMN (sacral spinal cord damage): large flaccid bladder
  • Detrusor dyssynchrony
  • Non-neurogenic
  • anatomic: ectopic ureter and patent uracus
  • functional: USMI, detrusor instability
216
Q

Treatment for UMN bladder

A
  • skeletal muscle relaxant
  • baclophen (GABAb agonist)
  • diazepam (GABAa agonist)
  • intraurethral atracurium (short active NMB)
  • smooth muscle relaxant
  • phenoxybenzamine (alpha 1 and alpha 2 antagonist)
  • bethanechol (M3 agonist)
217
Q

Urinary incontinence treatment

A
  • phenylpropanolamine: alpha1 agonist
  • estrogens: usually in combination with phenylpropanolamine

Combo successful in 88% of USMI cases

218
Q

when chosing the uretral cathere size the larger the better

A

False: the best choice is the smallest diameter achieving good urine flow

219
Q

What’s the landmark for catheter length?

A

Cranial aspect of ileal wing

220
Q

CAUTI incidence

A

10-52%
Much decreased when management protocol in place
20% females after 1off catheterization vs 0% males

221
Q

CAUTI risk factors

A

Mostly due to extra or intraluminal contamination from colonic or perineal flora or hands of medical staff
* age (increase of 20% by each 1y increase)
* length of catheterization (increase by 27% each 1 day longer)
* antimicrobial administration (increase of x4 times)

222
Q

What is the formula to calculate bladder volume on POCUS

A

W x average H x L x 0.2 x 𝜋

223
Q

Furosemide stress test

A

IV dose of 1.5-2mg/kg IV <200ml urine in 2h increased need for RRT and poorer prognosis

224
Q

Cut off values for UTI diagnosis free catch vs cystocentesis

A

> 10 5 for free catch
10 2 for cysto

225
Q

Urine osmolality and osmolar gap

A

Osmolality = 2 x [Na + K] + BUN + Glu
Osmolal gap = Measured osmolality - calculated osmolality
urine osmolality/serum osmolality < 10 mOsm/L

226
Q

Struvite uroliths

A
  • medically managed as due to infection
  • antibiotic and dissolution diet (acidify urine - pH<6.4)
  • should see a 30% reduction in size by 2-3 weeks
  • less dense and more angular than Caox on Xrays
    *
227
Q

Calcium oxalate uroliths

A
  • surgical condition
  • very bright on xrays
  • small breed dog (Bichons) predisposed
  • additional medical management long term with alkalinising diet, thiazides, potassium citrate (binds Ca in urine)
  • recurrence high despite optimal management (50% within 6y and 40% wihin 2y)
    *
228
Q

Urate uroliths

A
  • Dalmatian have genetic defect in uricase receptors (no conversion of uric acid into allantoin)
  • Allopurinol prevents conversion of hypoxantine and xantine into uric acid but key is low intake of proteins
229
Q

Cystine uroliths

A
  • medical treatment
  • genetic predisposition of Bulldogs
  • fancy diet with lots of animal protein (eggs and meat)
  • androgenic component so neutering helps
230
Q

Silica

A
  • rare
  • surgical condition
  • animals that eat dirt or diets rich in grains, husk and Mg
231
Q

In cats with obstructive upper urinary obstruction medical management should not be pursued as 90% are calcium oxalate

A

True

ureteral obstruction also is a medical emergency as there is a very rapid decline in renal function

232
Q

Approach to hypertension in dogs vs cats:

A
  • Dogs:
    1. ACEi
    2. ACEi+amlodipine
    3. ACEi+amlodipine + telmisartan
  • Cats:
    1. amlodipine or telmisartan
    2. amlodipine + telmisartan
233
Q

Approach to proteinuria

A
  • Dogs:
    1. diet + telmisartan
    2. telmisartan + ACEi
  • Cats:
    1. diet
    2. diet + ACEi or telmisartan

** antithrombotics **

234
Q

Why are ACEi not recommended as anti-hypertensive in cats?

A
  • Ineffectiveness: In cats, primary hypertension (idiopathic hypertension) is more common than in dogs, and the underlying mechanisms may not always involve the renin-angiotensin-aldosterone system (RAAS).
  • Alternative Activation of RAAS and aldosterone breakthrough: Cats may have multiple alternative pathways that bypass the inhibition of the classical RAAS by ACE inhibitors.
    Non-ACE pathways (like chymase) that can still convert angiotensin I to angiotensin II, leading to continued effects of aldosterone and the associated vasoconstriction and fluid retention.
235
Q

Cardio and renotoxicity of chronic activation of RAAS

A

Both AGII and aldosterone acts on tissue receptors inducing:
Fibrosis
* activation of fibroblasts
* increased transcription of nfkB
Endothelial dysfunction
* increased endothelin release
* decreased NOS
Tissue inflammation and remodeling
* Mineralcorticoid Receptor on macrophages –> M1 phenotype switch
Decreased sensitivity of baroreceptors
* decoupling of BP and HR with tachycardia and high BP (poor prognostic indicator in humans)

236
Q

Telmisartan

A

Selective AT1 receptor antagonist (also known as an angiotensin II receptor blocker, or ARB). It specifically blocks the angiotensin II type 1 (AT1) receptors, which mediate the effects of angiotensin II, such as vasoconstriction, aldosterone release, and sodium retention. While sparing beneficial action on AT2 (anti-inflammatory as Gs coupled so increased cAMP and vasodilatory)

237
Q

What is Entresto?

A

Entresto is the combination of ARB Telmisartan + neprilysisn (reduces brakedown of vasodilatory mediators like ANP and bradykinin).
Proven beneficial in B2 CHF dogs

238
Q

Key concepts highlighted by the canine remnant kidney model

A
  • compensatory hyperthrophy
  • hyperfiltration theory
  • inherhent progressive nature of canine CKD (proteinuria and systemic hypertension)
  • trade-off hypothesis (new with introduction of FGF-23)
239
Q

Hereditary nephropathy in dogs

A

Genetic defect in protein chains constituiting collagen type IV basement membrane

4 genetic defects leading to failure of synthesis of 𝜶4 and 𝜶5 chains (distruption of adult collagen 𝜶3𝜶4𝜶5 and keeping weak foetal one 𝜶1𝜶1𝜶2)

Severe proteinuria and CKD

240
Q

Familiar renal disease of soft coated wheaten terriers

A

Podocytopathy secondary to nephrin mutation
Often accompanied by PLE (unknown pathophysiology)

241
Q

Diagnosis of uroabdomen

A
  • Dogs:
    abdo crea/serum crea >2
    abdo K /serum K >1.4
  • Cats:
    abdo crea/serum crea >2
    abdo K /serum K >1.9
242
Q

What’s the reported recurrence rate for feline UO? and what are the major risk factors?

A

14-36%
* older age
* larger catheters
* short catheterization time
vs wet diet and access to outdoor associated with less recurrence

243
Q

Summary of RTAs types

A
244
Q

Formula to estimate bladder volume with POCUS

A

Bladder volume = length x width x ( average height) x 0.2 x 𝜋

245
Q

List 2 stress renal biomarkers

A

TIMP-2 and IGFBP7

They are cell arrest biomarkers. When renal tubular cells are exposed to stress and/or injury TIMP-2 and IGFBP7 are secreted to prevent further cell proliferation and provide the opportunity for DNA repair.

This usually happens 24-48h before sCr increase

246
Q

N-GAL origin and possible reason for its increase in urine

A

N-GAL is synthetized in the BM and stored in gelatinase neutrophilic granules, but it can also be expressed by stimulation of inflammatory cytokines by several tissues including the kidney, colon, trachea and lung epithelium.

N-GAL is freely filtered and completely re-absorbed by PT.

An increase in urinary N-GAL can be due to:
- PT damage and lack of reabsorption
- Pyuria
- Increased expression by inflammation of renal parenchyma

247
Q

Definition of furosemide resistance

A

Over 8-10mg/kg/day

Low urine sodium despite furosemide administration

Solution: add torasemide or substitute with torasemide (12-8 times less) or sequential nephron block (add thiazide)