Canine urolithiasis Flashcards

1
Q

Predisposing and risk factors

A
  • small breeds > large breeds
  • gender
  • diet and water consumption
  • increased Ca excretion (drugs, systemic disorders)
  • defects in purine metabolism
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2
Q

Diet and water consumption that predisposes to struvite formation

A

increased Mg, P

decreased water consumption

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3
Q

Diet and water consumption that predisposes to calcium oxalate formation

A

dry acidifying diet
increased Ca, oxalate, vit C
decreased water consumption

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4
Q

Diet consumption that predisposes to ammonium urate formation

A

increased purines (endogenous or exogenous)

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5
Q

Drugs that predispose to stone formation (increase Ca excretion)

A

urinary acidifiers
furosemide
glucocorticoids

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6
Q

Systemic disorders that predispose to stone formation (increase Ca excretion)

A
  • hypercalcemia: primary hyperparathyroidism (dogs), idiopathic hypercalcemia (cats)
  • Cushing’s disease (hyperadrenocorticism): glucocorticosteroids (increase mobilization of Ca from bone, decrease tubular re-absorption of Ca)
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7
Q

Predisposing and risk factors of Ammonium urate uroliths

A
  • portal vascular abnormalities
  • hepatic dysfunction
  • being a dalmation
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8
Q

Predisposing and risk factors of Xanthine uroliths

A

long term treatment with allopurinol

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9
Q

Diagnosis criteria

A
  • incontinence, dysuria, pollakiuria, anuria, hematuria
  • secondary microbial UTI (defective local host defense, foreign bodies in urinary tract)
  • palpation
  • rads or u/s
  • urinalysis: sediment (pyuria, hematuria, bacteria, crystals), pH, specific gravity
  • quantitative analysis
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10
Q

Crystalluria

A
  • it likely proceeds urolith formation, BUT not all animals with crystalluria form uroliths
  • uroliths can be present without crystalluria
  • type of crystal does not always relate to type of urolith
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11
Q

Oversaturation

A
  • unstable soln
  • crystals spontaneously precipitate (homogenous nucleation)
  • crystals aggregate and grow
  • crystals do not dissolve
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12
Q

Supersaturation

A
  • metastable soln
  • crystals do not spontaneously precipitate; precipitate on templates (heterogenous nucleation)
  • crystals may aggregate
  • inhibitors will impede or prevent crystallization
  • crystals do not dissolve
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13
Q

Undersaturation

A
  • stable soln
  • crystals do not precipitate
  • crystals do not aggregate or grow
  • crystals dissolve
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14
Q

Urolith formation

A
  • urinary retention
  • decreased concentration of crystallization inhibitors (for Ca oxalate inhibitors include: Mg, citrate, nephrocalcin, glycosaminoglycans)
  • once nucleation has occurred, crystal growth may occur at lesser degrees of supersaturation (metastable soln)
  • temperature change after urine collection induces crystal precipitation (so need to check for crystals in house)
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15
Q

A single diet can be formulated to be

A

undersaturated for struvite (treatment and prevention) and metastable for Ca oxalate (prevention)

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16
Q

Composition of struvites

A

Mg, NH4, PO4, occasionally Ca

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17
Q

Gross appearance of struvites

A

white to yellow, soft or hard, smooth or rough

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18
Q

Type specific characteristics of struvites

A

radiodense and form in alkaline urine

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19
Q

Gender, Age, concurrent disease, breed prevalence for struvites

A
  • female, 85-95% prevalence
  • 1-8 yrs (young adults)
  • UTI in 2/3 cases (infection induced struvite vs sterile struvite[sometimes in dogs but more often in cats])
  • mini schnauzer, bichon, shih tzu, mini poodle, lhasa apso (small breeds are commonly affected)
20
Q

Struvite formation

A
  • low water consumption, low urine volume
  • alkline pH
  • diet (directly relates to urine conc of Mg, PO4, [Ca])
  • urea (NH4 conc related to dietary protein)
  • disease (UTI- urease producing bacteria, staph, proteus)
21
Q

Dietary management of struvites (dissolution)

A
  • promote diuresis (urine SG <20%)
  • add dietary Na
  • acidify urine (pH 5.5-6.) with calculolytic diet (feed for 1 m after negative rads), supplemental acidifiers (dl-methionine or NH4Chloride)
  • control UTI (give abx as long as uroliths can be seen by rads, do not give abx if sterile struvites)
22
Q

Time for dissolution of urocystoliths (struvites)

A
  • literature says mean of 3.5 months (8-20 wks), but may see dissolution in 3-4 wks
23
Q

Time for dissolution of nephroliths (struvite)

A
  • 67-300 days, mean 184 days

use pH to help make educated guess, recheck in 2-3 wks to see if any changes in site in rads

24
Q

Precautions with calculolytic foods

A
  • increased NaCl concentration (caution with patients with CHF, CRF, hypertension)
  • patients at risk for pancreatitis (low protein/high fat diet)
  • protein levels too low for immature dogs, gestation, lactation (feed no longer than 2 wks)
25
Q

Prevention of struvites

A
  • prevent UTI! The diet will not prevent struvite urolithiasis if infection with a urease producing microbe is present
  • promote diuresis
  • ensure appropriate energy level
  • for sterile struvite: change diet composition and feeding patterns, +/- acidifiers to maintain urine pH 6.2-6.4
26
Q

Does the size of stones affect the length of time for dissolution

A

NO

27
Q

Composition of ammonium urate

A

NH4 and uric acid

28
Q

Gross appearance of ammonium urate

A

small, brittle, brown to green, concentric laminar rings on cross section

29
Q

Type specific characteristics of ammonium urate

A

radiolucent (will “hide” in rads)

form in acidic urine

30
Q

Gender, age, concurrent disease of ammonium urate

A
  • male (>85%)
  • <1 yr with portosystemic shunts (PSS), mean 3.5 yrs without PSS
  • PSS, liver disease, +/- UTI
31
Q

Breed predisposition for ammonium urate

A
  • dalmatian: only 30-40% of uric acid becomes allantoin, increased serum and urine levels of uric acid, autosomal recessive inherited possibly
  • english bulldog
  • mini schnauzers and yorkies b/c of PSS
32
Q

Ammonium urate formation

A
  • high urinary conc of urate (urate comes from monobasic ammonium salt of uric acid)
  • excess purines: oxypurines- hypoxanthine, xanthine, uric acid; aminopurines- (endogenous) adenine, guanine; methylpurines- caffeine, theophylline, theobromine
  • high urinary ammonium
33
Q

Dissolution of ammonium urate uroliths

A
  • promote diuresis
  • control UTI (when present)
  • restrict dietary protein (10-18%), purine
  • maintain a neutral - alkaline urine (pH 7.1-7.7), can give potassium citrate with meals if urine isn’t consistently alkaline
  • treat with xanthine oxidase inhibitor if urate excretion is >10 mg/kg/day
  • allopurinal (10-15 mg/kg) + purine restricted diet to minimize risk of xanthine stone formation
34
Q

Time for dissolution of ammonium urate

A

4-40 wks (mean 14.2 wks)

success rate 40%

35
Q

Prevention of ammonium urate

A
  • PSS surgery
  • feed low purine diet that promotes the formation of dilute alkaline urine (these diets are not appropriate for growth, lactation, gestation; high fat)
  • avoid acidifying high protein diets (these lead to excretion of amonium ions)
  • monitor daily urate excretion (goal is to have it reduced by 1/2 of pretreatment values)
36
Q

Composition of calcium oxalate stones

A

Ca and oxalic acid

37
Q

Gross appearance of calcium oxalates

A

small, hard, brittle, cream to tan to brown-green, smooth or sharp edged

38
Q

Type specific characteristics of calcium oxalates

A

radiodense (more than struvites, almost same as bone)

can form in slightly acidic to neutral urine

39
Q

Gender, age, breed predisposition for calcium oxaltes

A
  • males (>70%)
  • 6-12 yrs
  • mini schnauzer, lhasa apso, shih tzu, yorkies, mini poodle
40
Q

Calcium oxalate formation

A
  • calculogenic minerals do not = crystallization inhibitors
  • hypercalciuria: intestinal Ca hyperabsorption (believed to be cause in mini schnauzers), renal leak, excessive skeletal mobilization of Ca (resorptive)
  • hyperoxaluria: diet oxalates (veggie or grain sources), ascorbic acid, amino acids (glycine, serine), restriction of dietary Ca (increased GI oxalate absorption, so need to control levels of Ca and oxalate)
  • crystallization inhibitors: from soluble salts with Ca and oxalic acid (citrate, Mg, pyrophosphate), interfere with binding of Ca and oxalic acid (tamm-horsfall glycoprotein, nephrocalcin)
41
Q

Calcium oxalate prevention

A
  • cannot be dissolved!
  • reduce urine Ca and oxalate conc
  • avoid excessive dietary oxalates, vit C and D
  • restrict dietary protein (10-18%)
  • maintain adequate (moderate) dietary Ca (restriction increases intestinal absorption and urinary excretion of oxalate)
  • do NOT restrict P, this would increase Ca absorption
42
Q

Potassium citrate for prevention of calcium oxalates

A
  • through diet
  • urocit-K or polycitra-k at 50-150 mg/kg q 12 hrs
  • acts to sequester Ca from oxalate (Ca binds to citrate, Ca citrate is more soluble)
  • alkanalizes urine pH
43
Q

Thiazide diuretic for prevention of calcium oxalates

A
  • increases Ca resorption in proximal tubules

- hydrochlorthiazide at 2-4 mg/kg q 12 hrs for 2 wks

44
Q

Things that dietary management of calcium oxalate promotes

A
  • high concentration and activity of urolith inhibitors (avoid significant aciduria)
  • dilute urine: maintain SG<1.020, canned diet, add water to dry food, adding NaCl to food (not indicated in patients with CRF, cardiovascular dz)
45
Q

Cystine urolithiasis

A
  • cystinuria is an inborn error of metabolism
  • breeds: english bulldog, dachshund, basset hound, newfoundland
  • age: 2-5 yrs
  • radiodense
  • forms in acidic urine and becomes relatively soluble in alkaline urine
46
Q

Cystine urolithiasis dietary management and therapy

A
  • reduce dietary protein
  • promote diuresis (urine SG<1.020)
  • feed alkanalizing diet (potassium citrate, sustain pH ~7.5)
  • start with foods before adding drugs
  • thiol-containing drugs: d-penicillamine, N-(2-mercaptopropionyl)-glycine