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
Interpret: 1. TF/P = 1 2. TF/P < 1 3. TF/P > 1
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)
26
What is the consequence of no ADH in terms of urine concentrating ability?
Cells of the late distal tubule and collecting duct are impermeable to H2O Urine is dilute
27
Where is free H2O produced in the nephron
Diluting segments → TAL and early distal tubule
28
Where is ADH produced and stored?
1. Hypothalamus - supraoptic nuclei (majority) | 2. Posterior pituitary
29
At what positions do the liver and kidney hydroxylate vitamin D?
1. Liver → 25 → "25-OH-D (Calcidiol)" | 2. Kidney → 1 → "1,25(OH)2-D (Calcitriol)"
30
What substances are used to measure: 1. ECF 2. Plasma 3. Intersitial Fluid 4. ICF
1. Sulfate, Inulin, Mannitol 2. Evans Blue, RISA (Radioiodinated serum albumin) 3. Measure indirectly (ECF-plasma) 4. Measured indirectly (TBW-ECF)
31
How is renal plasma flow measured?
1. PAH - Filtered and secreted by renal tubules - Clearance of PAH measures effective RPF but underestimates true RPF by ~10%
32
What is the equation to calculate renal blood flow?
RBF = RPF/(1-HCT) RPF = PAH clearance
33
What is the equation used to calculate GFR (starling equation)? What does a (+) value indicate?
GFR = Kf [(P(GC)-P(BS)) - (π(GC) - π(BS)] (+) = filtration is favored
34
Where is glucose reabsorbed in the nephron? How is this accomplished?
1. Early proximal tubule | 2. Na-Glucose co-transport
35
What is the MOA of ANP in RAAS inhibition?
1. Stimulus → dilution of the atria 2. Effects - Inhibit renin release - Inhibit action of angiotensin II - Inhibits Na reabsorption
36
What is the plasma osmolality equation?
2(Na+K) + Glucose/18 + BUN/2.8 Osmolality = # of osmoses per kilogram of solvent
37
How does ECF volume affect proximal tubular reabsorption
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
38
What are the mechanisms of K reabsorption and secretion in the distal tubule and collecting duct?
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
39
How does ADH affect urea regulation?
Acts on UT-A1 and UT-A3 transporters Increases urea in the interstitial → increases concentrating ability
40
What stimulates ADH secretion?
1. Increase plasma osmolality - Osmoreceptors in anterior hypothalamus 2. Decrease atrial pressure/blood volume - Baroreceptors
41
What is the relationship between BUN and serum creatinine in prerenal azotemia? Why?
1. BUN increases more than creatinine | 2. Hypovolemia increases urea reabsorption in the proximal tubule
42
1. How are weak acid and weak base forms affected by: a. acidic urine b. alkaline urine 2. How does this affect their excretion?
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
43
What is the mechanism of phosphate reabsorption in the proximal tubule?
Na-Phosphate cotransport
44
What inhibits phosphorous reabsorption in the proximal tubule? How?
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
45
How do the following affect Ca excretion/resorption in the nephron? 1. Loop diuretics 2. PTH 3. Thiazide diuretics
1. Increase excretion in the LoH 2. Increase reabsorption in the distal tubule 3. Increase reabsorption in the early distal tubule
46
Where is magnesium reabsorbed in the nephron?
* 85-90% reabsorbed 1. LoH - 65% (mostly from thick) 2. Proximal tubule - 25% 3. Distal convoluted tubule and collecting duct - <5%
47
Where does PTH act in the nephron?
1. Thick limb of the LoH | 2. Distal convoluted tubule and collecting duct
48
What are the transport mechanisms for Na in 1. Early proximal tubule 2. Distal proximal tubule
1. Cotransporters → glucose, amino acids, phosphate, and lactate Countertransport → Na-H exchange linked to HCO3 reabsorption 2. Reabsorbed with Cl
49
What are the transport mechanisms for Na in 1. Thick ascending LoH 2. Early distal tubule 3. Late distal tubule
1. Na/K/2Cl cotransporter 2. Na/Cl cotransporter 3. Na Channels (stimulated by aldosterone)
50
What are the different vasopressin receptors?
1. V1A → vascular smooth muscle → vasoconstriction 2. V2 → collecting ducts → insert aquaporin 2 channels 3. V3 → anterior pituitary → ACTH release
51
What causes renal arterioles to 1. Vasoconstrict 2. Vasodilate
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
52
Where is urea reabsorbed in the nephron?
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
53
What are the different urea transporters?
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
54
Reabsorption of filtered HCO3 occurs primarily in which nephron segment?
Proximal tubule
55
What is the carbonic anhydrase equation?
CO2 + H2O -> H2CO3 -> carbonic anhydrase -> H + HCO3
56
What is the net result of bicarb reabsorption in the proximal tubule?
1. Net reabsorption of filtered HCO3 | 2. Does not result in net H+ secretion
57
What regulates reabsorption of filtered HCO3
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
58
In what forms is H+ excreted?
1. Titratable acid (H2PO4) | 2. NH4
59
What determines the amount of H+ excreted as a titratable acid?
1. Amount of urinary buffer (usually HPO4) | 2. pK of the buffer
60
What determines the amount f H+ excreted as ammonium?
1. NH3 synthesized by renal cells | 2. Urine pH
61
How/where is NH3 produces in the kidney? What inhibits this process?
1. Produced in renal cells from glutamine | 2. Hyperkalemia inhibits NH3 synthesis
62
What is the underlying cause of metabolic acidosis?
Overproduction/ingestion of acid OR Loss of base = decrease in [HCO3]a → acidemia
63
What are consequences of a metabolic acidosis?
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
64
What is the underlying cause of a metabolic alkalosis?
Loss of [H+] OR Gain of base → increase arterial [HCO3] → alkalemia
65
What are the consequences of a metabolic alkalosis?
1. Hypoventilation → respiratory compensation | 2. Increased excretion of HCO3 → filtered load of HCO3 exceeds the kidneys ability to reabsorb it
66
What is contraction alkalosis?
Metabolic alkalosis is accompanied by ECF volume contraction (vomiting) → reabsorption of HCO3 increases due to ECF volume decrease and activation of RAAS → worsens alkalosis
67
What is the underlying cause of respiratory acidosis?
Decreased ventilation and retention of CO2 → increased arterial CO2 → increased H+
68
How does the kidney compensate for respiratory acidosis?
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
69
What is the underlying cause of respiratory alkalosis?
Increased ventilation → loss of CO2 → decreased H+
70
How does the kidney compensate for respiratory alkalosis?
Decreased excretion of excess H, decrease reabsorption of HCO3 *Takes time, only occurs in chronic cases
71
What are the effects of hypoaldosteronism on the kidney
1. Decrease Na reabsorption 2. Decrease K secretion 3. Decrease H secretion
72
What stimulates the production of erythropoietin? How long does it take for HCT to increase?
1. Epi, Norepi, prostaglandins, and HIF1α | 2. 5 days
73
What happens when the macula dense senses a decrease in the NaCl in the distal tubules
1. Dilates afferent arterioles → increase RBF and GFR | 2. Causes renin release from JG cells → RAAS
74
Where does aldosterone act in the kidney? Where is the primary site of action?
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
75
What are the actions of Angiotensin II?
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
76
What is the equation for filtration fraction? how much is normally filtered?
Filtration fraction = GFR/Renal plasma flow ~20% of plasma
77
What increases Ca reabsorption in the nephron?
1. Acidosis 2. Increase PTH 3. Decrease ECF volume 4. Increase BP 5. Increase Vit D3
78
What buffer system is most important 1. Extracellularly 2. Tubular fluid 3. Intracellularly
1. HCO3 2. Phosphate 3. Phosphate
79
Hyperaldosteronism acid/base status
Metabolic alkalosis → Increase H+ secretion
80
2/3 of filtered H2O is reabsorbed in which part of the nephron?
Proximal tubule
81
What is the equation for free water clearance?
Urine flow rate - osmolar clearance Osmolar clearance = (urine osmolarity x urine flow rate)/plasma osmolarity
82
What is nephrotic syndrome?
1. Peripheral edema 2. Proteinuria 3. Hypoalbuminemia 4. Hypercholesterolemia
83
Cats with FIC have increased levels of what?
1. Tyrosine hydroxylate in the hypothalamus | 2. Plasma norepinephrine levels
84
What are the diagnostic criteria for renal tubular acidosis?
1. Normal to near normal GFR | 2. Hyperchloremic, normal anion gap, metabolic acidosis without GI disease
85
Indications for a renal diet
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
What are the major side effects of glomerular disease?
1. Edema 2. Hypertension → 80% of patients 3. Thromboembolic events → 5-15% of patients 4. Hyperlipidemia
87
What kind of uroliths can be dissolved?
Struvite, cysteine, and urate
88
What % of lyme positive dogs have proteinuria?
<2% 95% of lyme seropositive dogs show no signs of illness
89
What are causes of decreased iCa?
1. Alkalosis → important 2. Lipemia 3. Increase BP/ECV 4. Decrease PTH
90
What are the causes of acquired Fanconi syndrome?
1. Gentamycin 2. Ethelyne glycol toxicity 3. Primary hypoparathyroidism
91
What are some complications associated with recurrent UTI
1. Polypoid cystitis 2. Emphysematous cystitis → commonly associated with E. coli 3. Struvite uroliths 4. Pyelonephritis
92
What are the indications of underlying glomerular disease?
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
How can calcium oxalate stone recurrence be prevented?
1. Potassium citrate | 2. Thiazide diuretics
94
What is the treatment of cystine stones?
2MPG + Alkaline urine (potassium citrate or bicarb) + protein restriction
95
What are the underlying causes for struvite stones?
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
What are the components of purine stones?
Urate and xanthine
97
How common are calcium oxalate stones?
1. 40% of all canine uroliths 2. Male predisposition 3. More common in small breeds
98
What increases the risk of calcium oxalate stones?
1. Hypercalcinuria - Due to increase intestinal reabsorption, increased bone resorption, or primary renal Ca leak 2. Common with hyperparathyroidism
99
How are purine stones treated?
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
Describe purine metabolism
Purine catabolism → hypoxanthine → xanthine oxidase → xanthine → xanthine oxidase → uric acid → urate oxidase → allantoin
101
What are calcium phosphate uroliths composed of and what disease process are they associated with?
1. Hydroxyappetite | 2. Hyperparathyroidism (30-40% will develop)
102
How common are uroliths in cats?
10-15% of cats with lower urinary signs with uroliths
103
What are the most common uroliths in the cat?
1. Calcium oxalate - similar process as dogs | 2. Struvite
104
What % of intact male dogs have BPH?
75%
105
What is the treatment of choice for BPH?
Castration * 50% reduction in 3 weeks * 75% reduction in 3 months
106
What is the equation for free water deficit?
Weight(present) X ((PNA(present)/PNA(previous)) - 1) * If you dont know the previous Na, assume high end of normal (145)
107
Dogs with PLE have altered amounts of which amino acids?
1. Asparagine 2. Glycine 3. Proline 4. Serine 5. Tyrosine
108
What are the results of glomerular hypertension?
1. Increased single nephron GFR | 2. Enlarged radii of the pores of the filtration membrane
109
Survival time for azotemic nephrotic syndrome
<60 days
110
When should immunosuppressive therapy be considered for dogs with glomerular disease?
1. Serum creatinine > 3.0 2. Azotemia is progressive 3. Hypoalbuminemia < 2.0 * Assess response to therapy in 8-12 weeks
111
What is the most powerful stimulus for aldosterone?
Hyperkalemia
112
What would you expect in a patient with increased bicarb and decreased K
Paradoxical aciduria
113
What are the differentials for hyperosmotic urine?
1. SIADH 2. H2O Deprivation 3. Volume depletion
114
What produces prostaglandins and what do they do?
1. PGE2 produced by type 1 medullary interstitial cells | 2. Increase cortical blood flow and decreased medullary blood flow
115
Effects of loop diuretics in the context of AKI
1. Increase urine production 2. Decrease energy requirements without increase GFR * Work in 20-60 min
116
Mechanisms of reduced GFR in AKI
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
What are the most common causes of CKD in dogs
1. Tubulointerstitial nephritis (60%) 2. Glomerulonephritis (30%) 3. Amyloidosis (7%)
118
What is the difference between type 1 and type 2 renal tubular acidosis?
1. Type 1 → Distal, cannot secrete H+ by intercalated cells | 2. Type 2 → Proximal, cannot reabsorb bicarb
119
How do you treat membrinoproliferative glomerulonephritis in the dog?
1. Aspirin → because platelet activation and TXA2 induced vasoconstriction would promote progression 2. Glucocorticoids → for immunosuppression
120
What is the underlying cause for hereditary nephritis?
Collagen IV deficit results in leaky glomerular basement membrane
121
What is the most common form of glomerular disease in the dog?
Membranoproliferative glomerulonephritis *Occurs commonly secondary to antibody complexes from Borrelia burgdorferi → immune complexes deposit on subendotheilial glomerular basement
122
How is amyloidosis different in Shar Peis?
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
Routin UTI screening is recommended for cats with which risk factors?
1. Recent catheterization 2. PU surgery 3. Diabetes mellitus 4. Renal failure 5. Hyperthyroidism
124
What is the treatment for struvite stone?
Antibiotics + acidic urine Takes ~3 months to dissolve
125
What is the treatment for urate stones?
Allopurinol + alkaline urine (bicarb or potassium citrate) + protein restriction
126
What is the treatment for calcium oxalate stones?
Surgery is the only option! They will not dissolve!
127
How frequently do calcium oxalate stones recur?
Dogs: 50% within 3 years
128
How common are struvite stones?
40% of canine uroliths
129
What are the most common breeds for purine stones? Why?
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
How do you prevent purine uroliths?
Lower protein diet that promotes dilute urine Vegetarian diets are a good choice
131
What is the underlying cause of cystine stones?
1. Uncommon 2. Due to proximal tubular defect in cystine reabsorption 3. Recurrence is common
132
How are struvite uroliths different in the cat?
Found in STERILE urine with an ALKALINE pH Can dissolve in 1 months with an acidifying diet
133
What are the two forms of FIC? Which is the most common?
1. Ulcerative → 10% | 2. Non-Ulcerative → 90%, very common
134
How does FIC cause obstruction?
1. Urethral plugs (60%) | 2. Urethrospasm (30%) → functional obstruction
135
What kind of crystals form in FIC?
1. Albumin and struvite | * Struvite associated with increased pH caused by inflammation
136
What is the most common cause of urinary incontinence in female dogs?
1. Urethral sphincter mechanism incompetence - Develop increased collagen and decreased muscle fibers 2. Detrusor instability is a less common cause
137
How is urinary incontinence treated in dogs?
1. α adrenergic agonists → improves tone - Phenylpropanalomine (90% effective) 2. Estrogen → Increased # of α receptors - Estrogen 50% effective * Can be used together
138
What is the most common causative agent for acute bacterial prostatitis?
E. coli (70%)
139
Dogs with acute bacterial prostatitis are usually (symptomatic/asymptomatic)
Symptomatic
140
Treatment of choice for acute bacterial prostatitis?
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
Dogs with chronic prostatitis are (symptomatic/asymptomatic)
Asymptomatic
142
Nephrogenic diabetes insipidus is often secondary to what?
1. V2 receptor interference | - Drugs, Endotoxins, or Electrolyte Disorders
143
At what point do neurologic signs associated with hypernatremia develop?
Na > 170
144
Causes of false positive proteinuria on dipstick
1. Urine pH >= 7.5 | 2. Highly concentrated urine
145
What % of proteinuria dogs with bacteruria, pyuria, and lower urinary tract disease would have missed bacterial growth if cultured?
1.8% → Grimes 2020 JVIM
146
How is colchicine metabolized?
Cytochrome p450 *This is an MDR1 substrate
147
What are the effects of using an ACEi?
1. Dilation of efferent arterioles - Decrease GFR - Decrease proteinuria
148
What is the goal when starting an ACEi
1. Achieve normal UPC or decrease UPC by 50% | * Wait 1 month before rechecking
149
Which receptor(s) is blocked by angiotensin II receptor blockers?
1. Angiotensin II type 1 receptors (AT1) | - Do not block AT2
150
What are the roles of the following receptors? 1. AT1 2. AT2
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
What is indicated by a metabolic acidosis with normal anion gap?
1. Cl increased | - Occurs with diarrhea or renal tubular acidosis
152
Urinary fractional excretion <1% is most consistent with what?
Dehydration/Prerenal azotemia
153
What is a risk of a DDVAP trial in a dog with psychogenic polydipsia?
Hyponatremia
154
What are the criteria for central diabetes insidious?
1. Dilute urine despite strong osmotic stimuli for ADH release 2. Absence of renal disease 3. Increase osmolality following ADH administration
155
How are calcium oxalate stones prevented?
Adequate hydration
156
What drug increases the osmolar gap?
Mannitol
157
Cats with membranous glomerulonephritis have improved survival if?
1. IgG or C3 deposition → compared to those with IgM or IgA or higher stage
158
Which enzyme (other than ACE) can produce angiotensin II?
Chymase
159
Which type of RTA has: 1. Alkaline urine despite metabolic acidosis 2. Lower fractional excretion of HCO3 3. Higher fractional excretion of HCO3
1. Type 2 2. Type 1 3. Type 2
160
Effect of diltiazam in context of AKI
May help to stabilize membrane and improve renal blood flow
161
3 most common causes of AKI
1. Toxic 2. Ischemic 3. Infectious
162
Effects of mannitol in context of AKI
1. Increase GFR 2. Relieve tubular obstruction 3. Decrease local energy requirements
163
What are the consequences of decreased oxygen supply in the context of AKI
1. Inability to power Na-K ATPase → cellular swelling → death
164
AKI is considered to be a creatinine increase of ___ from baseline
>0.3 mg/dl
165
Pyelonephritis is most commonly associated by gram (+/-). Which organism is most common?
1. 75% are gram - | 2. 40% of all UTIs caused by E. coli
166
AKI: Most common toxins 1. Dog 2. Cat
In order of frequency 1. Ethelyne glycol, NSAID, Vit D3, Aminoglycosides 2. Ethelyne glycol, Vit D3, Lilies
167
What kind of abs is recommended for the best renal penetration?
1. Fluoroquinolones | * Potentiated pencilling have moderate renal penetration
168
If hypokalemia refractory to K supplementation, consider ___ supplementation
Magnesium
169
Consequences of mannitol administration for AKI in 1. Dehydrated patient 2. Overhydrated patient
1. Worsen intracellular dehydration | 2. May drive pulmonary edema
170
What is the only acute way to decrease phosphorous (AKI)
Dialysis | *Phosphate binders prevent absorption from food
171
Definition of CKD
1. Kidney damage that has existed for >3 months with or without decrease GFR OR 2. Decrease GFR by >50% for >3 months
172
Most common causes of CKD in cats
1. Tubulointerstitial nephritis (70%) 2. Glomerulonephritis (15%) 3. Lymphoma (10%) 4. Amyloidosis (2%)
173
What are the characteristics of a renal diet?
1. Low protein 2. Low phosphorous 3. High omega 3
174
Hypertension promotes progressive CKD by
Worsening proteinuria
175
What is the most common type of glomerular disease in the dog? What are its subtypes? The cat?
1. Membranoproliferative glomerulonephritis - Type 1: Subendothelial IC deposition - Type 2: Intramembranous IC deposition (uncommon) - Type 3: Subepithelial IC deposition 2. Cat: Membranous glomerulonephritis
176
What is Fanconi Syndrome?
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
What are ACEi used to treat glomerular disease?
1. Reduce intraglomerular pressure a. Reduces proteinuria b. Delays onset of renal failure
178
Why do thromboembolic events occur in glomerular disease?
1. Believed to be secondary to ATIII loss 2. More likely to occur if albumin < 2 3. PTE is most common
179
What is the most common form of glomerular disease in the cat?
Membranous nephropathy → second most common in dogs * Typically idiopathic * Immune complex deposition on the sub epithelial glomerular basement membrane and podocyte (urine)
180
Proteinuria and nephrotic syndrome status in membranous nephropathy
1. Proteinuria → severe | 2. Nephrotic syndrome → common
181
How is membranous nephropathy treated?
Immune suppression 1. Chlorambucil and prednisone 2. Cyclosporine
182
What is the prognosis for membranous nephritis?
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
What is the cause of amyloidosis?
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
Proteinuria and nephrotic syndrome status in amyloidosis
1. Proteinuria → severe | 2. Nephrotic syndrome → common
185
How is amyloidosis treated?
1. Colchicine 2. May help reduce development of renal amyloidosis but wont reverse it 3. Decreases serum amyloid A from the liver
186
What is glomerulosclerosis?
1. End stage changes resulting from early glomerulonephritis | 2. Glomerular membrane is too thick to function
187
What CFU counts would be indicative of infection for the following collection methods? 1. Cysto 2. Catheter 3. Free Catch
1. >1,000 2. >1,000 (cat), >10,000 (dog) 3. >10,000 (cat), >100,000 (dog)
188
What is the prognosis for amyloidosis?
Poor | *Only 8% survive >1 year
189
What are the antibiotics of choice for empiric UTI treatment?
1. Amoxicillin | 2. TMS
190
What is the most common causative agent for fungal UTI? How is it treated?
1. Candida - Aspergillus and cryptococcus are also possible 2. Fluconazole