Urolithiasis
- A urolith is a polycrystalline concretion found in the urinary
tract, containing primarily inorganic crystalloids and a small amount of
organic matrix. Uroliths have an organized and regular pattern of
crystal deposition on the organic matrix. Uroliths are also called
calculi or stones.
- Microscopic or macroscopic precipitates of crystals in a
disorganized fashion are NOT uroliths but are simply called
crystalluria.
- Nephroliths are uroliths in kidney.
- Cystic calculi are uroliths in bladder.
- Matrix is the organic component of a urolith.
Uroliths consist of concentric layers of crystalline (mineral) aggregates
on an organic matrix. More than one crystalline component may be present in
uroliths. Uroliths are named by their predominant crystalline component. The
organic matrix is composed of protein and muco protein and generally
constitutes < 5% of the urolith.
Uroliths can occur in dogs of any age. Uroliths overall occur more
frequently in females (72%) than in males (28%) but metabolic uroliths occur
more commonly in males.
There are 3 primary factors which contribute to urolith formation:
- supersaturation of urine with minerals leading to crystalluria.
Urine may be supersaturated with crystals due to increased dietary
intake of those crystals, reduced solubility of crystals due to pH,
concentrated urine enhancing crystal concentration or congenital
abnormalities resulting in the presence of abnormal crystals in the
urine
- delayed passage of crystals through the urinary tract. Crystal
elimination may be delayed due to adherence of crystals to damaged
mucosa, stationary foreign bodies (i.e., suture), sludging in an atonic
bladder, or in a urachal diverticulum. A calculus of one mineral type
may act as a stationary foreign body upon which minerals of a different
type may deposit .
- reduction of normally present inhibitors of crystal growth and
aggregation (i.e. citrate, pyrophosphates).
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The clinical presentation of an animal with urolithiasis depends upon the
location of the uroliths. Uroliths can lodge in the urethra of the male dog,
but rarely lodge in the urethra of bitches as the female urethra is shorter
and more distensible. Uroliths usually lodge at the two narrowest regions of
the male urethra; the caudal aspect of os penis and the point at which the
urethra curves around the ischium of the pelvis (called the ischial arch).
The urethra is less distensible in these two locations and uroliths will
result in partial or total obstruction.
Clinical signs associated with urethral obstruction may include:
- frequent attempts to urinate producing small amounts of urine
- straining to urinate (stranguria or dysuria)
- inability to urinate (anuria) if the obstruction is complete
- paradoxical incontinence. The animal may
unconsciously dribble urine past a partial obstruction
- hematuria
- over-distended urinary bladder
- rupture of the urinary bladder resulting in ascites
- signs of postrenal uremia
Cystic calculi (bladder location) without obstruction
result in signs including:
- dysuria/stranguria
- hematuria
- pollakiuria
- the bladder is small due to the frequent voiding
- systemic signs are usually absent
Renal or ureteral calculi may result in the following signs:
- abdominal pain
- hematuria
- hydronephrosis causing renal enlargement may occur if the calculus
obstructs urine flow
- systemic signs of anorexia, depression and fever may occur if a UTI
accompanies the calculus
Animals with bladder or renal calculi may be asymptomatic.
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Laboratory
The laboratory evaluation of many patients with non-obstructive
urolithiasis is usually normal. Leukocytosis may
be observed if there is an acute infection of the kidneys or prostate.
Anemia may be present due to blood loss or due to the anemia of chronic
inflammatory disease . If the animal has an obstruction, serum biochemical
abnormalities are those of post renal obstruction. Patients with calcium
oxalate calculi may be hypercalcemic.
Urinalysis often discloses
- hematuria
- pyuria due to inflammation or infection
- proteinuria from blood or inflammation or infection (secretory/post
glomerular proteinuria)
- crystalluria
- bacteria if UTI is present
- isosthenuria may be present if concurrent pyelonephritis led to
renal dysfunction. Isosthenuria may also reflect an under lying disease
that led to stone formation such as liver disease which may result in
urate uroliths and dilute urine.
The urine pH is variable and may provide a clue as to the type of urolith
present
- struvite uroliths form in alkaline urine
- calcium oxalate uroliths form in acid urine
Crystals in the urine represent a risk factor for urolithiasis but are
not proof positive that uroliths are present. Animals can have crystals
without having uroliths and some animals with uroliths do not have crystals
in the urine. The significance of crystals is as follows:
- magnesium, ammonium phosphate (struvite) crystals may indicate the
presence of struvite uroliths but can be seen in the urine of normal
animals
- ammonium urate crystals can be seen in the urine of animals with
portal vascular anomalies, severe hepatic disease, or normal Dalmatians
- calcium oxalate crystals can be seen in the urine of normal animals,
ethylene glycol intoxicated animals, animals with calcium oxalate
calculi or hypercalcemic animals
- cystine crystals are always abnormal and indicate an impaired
ability of the renal tubules to reabsorb the amino acid cystine
In vitro variables may affect the formation or dissolution of crystals in
vitro. Evaporation, pH changes, and temperature all may all affect the
appearance or disappearance of crystals. Analysis of fresh urine will
provide a better indicator of the degree of crystal saturation in vivo.
Drugs including sulfonamides, contrast agents, ampicillin, and primidone may
precipitate as crystals in the urine. Urine crystals that form while
patients are consuming diets fed in the hospital may be different than the
urine crystals formed by patients fed in the home environment.
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Radiology
The radiographic appearance of calculi depends on the size and mineral
composition of the urolith(s). Based on mineral content, calcium oxalate,
struvite, and silica are almost always radio opaque. Very small uroliths of
radio dense minerals may be over-looked on radiographic examination. Cystine
and ammonium urate are less radio opaque and may require contrast studies to
be seen. If they are moderate to large in size then they may be seen without
contrast.
If uroliths are found in one portion of the urinary tract, other parts of
the urinary system should also be evaluated radiographically for calculi.
Radiographic evaluation may also disclose predisposing or complicating
abnormalities. Ultrasound can also be used to detect calculi in both the
bladder and kidneys.
The qualitative and quantitative mineral composition of calculi should be
determined to help formulate prophylactic measures to prevent recurrence
after surgical removal of the calculi or to institute medical dissolution. A
urolith should be broken (by the lab performing the
analysis) and the center of the calculus should be evaluated
separately from the outer layers as the nidus (center) may differ in mineral
composition from the outer layers. A commercial kit is available--the Oxford
stone analysis kit--but the kit will not detect xanthine or silica, and has
been reported unreliable in consistently detecting calcium.
Commercial laboratories will perform stone analysis by crystallographic
methods which provide the percentages of all mineral types which comprise
the stone.
-
Urolithiasis Laboratory
College of Veterinary Medicine
University of Minnesota
St. Paul, Minnesota
- Urolithiasis Laboratory
- PO Box 25375
- Houston, TX 77005
- Urinary Stone Analysis Laboratory
- Dept of Medicine
- School of Veterinary Medicine
- University of California
- Davis, CA 95616
Cultures should be obtained from both the center
and outer layers of the urolith. If the animal has
recently received antibiotics, the urine and the external surface of the
uroliths may be sterile but the center may still harbor bacteria, indicating
that bacterial infection was present at the onset of stone formation and may
have contributed to stone formation.
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Struvite is composed primarily of magnesium ammonium
phosphate but may be impure, containing minor quantities of
calcium phosphate. Other names for struvite uroliths include
phosphate calculi, triple phosphate stones, and infection
stones. Struvite uroliths are the most common type of calculi
occurring in dogs. They can affect any age animal and are more
common in female dogs. The breeds most commonly affected are the
miniature schnauzer, miniature poodle,
Shih Tzu, Bichon Frise, Lhasa Apso, Cocker
spaniel and mixed breed dogs.
Most struvite calculi occur in the lower urinary tract (~95%)
but they may occur in the upper urinary tract or in multiple
locations. |
There are several factors which promote development of struvite uroliths
including:
- alkaline urine
- increased mineral concentration
- concentrated urine
- genetic predisposition
UTI with urease producing bacteria (urease catalyzes the conversion of
urea to ammonia and bicarbonate ) results in
alkaline urine and increases the concentration of ammonium ion in urine.
Staphylococcus, proteus, and
ureaplasma are urease producing bacteria. Less
common urease-producing organisms that infrequently cause struvite
uroliths include Pseudomonas and Klebsiella.
Most, but not all dogs with struvite uroliths have a UTI.
Experimentally produced urinary tract infections have resulted in struvite
calculi formation in 2-8 weeks (average = 4.5 weeks).
Struvite
crystals are less soluble in alkaline urine and are more likely to
precipitate on an organic matrix as uroliths. Other causes of alkaline urine
include drugs such as sodium bicarbonate, renal tubular acidosis in which
bicarbonate is lost in the urine resulting in systemic acidosis, and diets
high in cereal proteins.
Concentrated urine and increased amounts of crystals in the urine
increases the probably of crystals aggregating to form uroliths.
There is a high frequency of occurrence of struvite uroliths in Miniature
Schnauzers suggesting a genetic predisposition.
The gross appearance of struvite uroliths may be smooth or spiked like a
jack.
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Treatment
of patients with struvite uroliths
If urethral obstruction is present, the obstruction should be removed by
hydropropulsion of the urolith(s) into the bladder. If the urethral stone
cannot be dislodged, a urethrotomy must be performed to alleviate the
obstruction.
Struvite uroliths in the bladder can be treated by surgical removal or
medical dissolution. Small uroliths may be missed during surgery so medical
dissolution measures are advised for 3-4 weeks post surgical to dissolve any
remaining small uroliths. Postoperatively a urolith should be analyzed for
chemical composition and a bacterial culture performed.
Surgical candidates include patients with obstruction that cannot be
corrected by nonsurgical means, patients with anatomic defects of the
urogenital tract that predispose to urolithiasis and are amenable to
surgical correction, poor client compliance with therapeutic recommendation
and patients with stones that are not decreasing in size in response to
medical measures.
In order to initiate medical dissolution of uroliths, you need to have
some information regarding the mineral type of the urolith. "Guess-timate"
of mineral type is made upon
- radiographic density
- alkaline urine pH
- struvite crystals
- urinary tract infection especially with staphylococcus or
proteus
- analysis of any stones voided. You may catch small stones in a
screen fish net as they are voided, or may aspirate small stones with a
catheter.
- frequency of occurrence in the breed
- history of uroliths in related animals
The goal of medical management
is to promote dissolution by inducing undersaturation of urine with minerals
causing the minerals in the uroliths to go into solution. The components of
medical management are:
- Administer antibiotics based on urine culture for as long as
uroliths are visible radiographically and for one additional month.
- Feed a calculolytic diet (SD- Hills) until uroliths are no longer
radiographically visible and for one additional month. SD diet has the
following attributes:
1. reduced protein. Less protein in the diet
results in less urea in the urine and less ammonia &
bocarbonate production by urease producing bacteria. There is less
ammonia to contribute as a substrate of struvite uroliths as well as less effect
on increasing urine pH.
2. reduced magnesium and reduced phosphorus which are the mineral
substrates of struvite uroliths
3. high salt to promote diuresis and dilute crystals
4. production of acid urine which makes struvite crystals more
soluble
It is important to feed ONLY the calculolytic diet. Owner and animal
compliance can be evaluated. If the protocol was followed properly the BUN
will be <10 mg/dl, urine pH < 6.5, and urine SG < 1.015.
If UTI persists despite appropriate antibiotic therapy, acetohydroxamic
acid can be added to the treatment regime. Acetohydroxamic acid is a urease
inhibitor. It is dosed at 25 mg/kg/day divided in 2 doses.
Potential side effects include:
- teratogenesis
- hemolytic anemia
- abnormal bilirubin metabolism.
During medical treatment, monitor the patient monthly including BUN,
albumin, urinalysis, and abdominal radiographs. Stones dissolve in 8-20
weeks (mean = 3.5 months). If there is no change in the size of uroliths in
8 weeks, the stone is probably not struvite or is refractory to dissolution
and surgery should be performed. For those patients who show regression in
size of the stone, continue medical therapy for 1 month after the stone can
no longer be visualized on radiographs.
If the urine is sterile, then feed only the calculolytic diet without
antibiotics. Use this protein restricted diet in growing pups with caution.
Severely protein restricted diets such as SD should not be fed long term as
hypoproteinemia may develop.
The recurrence rate of struvite uroliths is 21 - 25% if a prophylactic
measure is not implemented.
Methods to prevent reoccurrence include:
- Early identification and treatment of UTI. Have the owner monitor
urine pH on the first urine voided in the morning, once a week. If the
urine is alkaline then it should be cultured to identify UTI early,
before stones reoccur.
- If urine remains alkaline despite antimicrobial therapy, the diet
can be changed to promote formation of acid urine or an acidifier can be
administered without a change in diet. Hills CD is mildly protein
restricted, mineral restricted, and promotes acid urine. SD is too low
in protein for long term use and will result in protein depletion if
used long term. Many of the breeds predisposed to struvite urolithiasis
are also predisposed to calcium oxalate urolithiasis. In these breeds,
dietary therapy to prevent struvite urolithiasis that includes urinary
acidification and magnesium restriction (such as
Hills CD) could contribute to formation of calcium oxalate
urolithiasis later in life. Diets such as Waltham
Canine S/O Lower Urinary Tract Support Diet which are designed for
prevention of both struvite and calcium oxalate urolithiasis may be fed
long-term in breeds predisposed to both stone types.
- The diet can be salted to encourage increased water intake and
formation of dilute urine to dilute crystals but chronic salt
administration can predispose to development of hypertension
or worsening of renal function in patients with renal disease. The role
of salt in stone prevention is undergoing evaluation.
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Calcium oxalate uroliths are
the second most common stone type occurring in dogs.
They occur most often in middle aged to older dogs
(except Bichon Frise seem to be affected at a
younger age). They occur more commonly in male dogs (~70%). Neutered
male dogs have increased risk compared with intact
dogs. A contribution to development may be the
reduction of estrogens and increase in testosterone which occurs with
advancing age. Estrogens increase the concentration of citrate in the urine
and decrease the excretion of calcium. As estrogens decrease, the opposite
situation exists which is a reduction in urine citrates and an increase in
urine calcium. Testosterone may increase hepatic oxalate production.
Oxalate calculi usually occur in the bladder and urethra in dogs compared
to humans which more often develop renal oxalate
uroliths.
Breeds most commonly developing calcium oxalate uroliths:
Schnauzers
Lhasa Apso
Yorkshire terriers
Bichon Frise
Shih Tzu
Miniature poodles
Pomeranian
Cairn terrier
Maltese
Chihuahua
Factors which may predispose
to calcium oxalate uroliths include:
- hypercalcemia from primary hyperparathyroidism, vitamin D
intoxication, osteolytic neoplasia, or pseudohyperparathyroidism.
Only about 4% of dogs with calcium oxalate stones have an elevated blood
calcium.
- hypercalciuria with normocalemia (most animals with calcium oxalate
calculi are normocalcemic) due to increased intestinal absorption of
calcium and decreased renal tubular reabsorption of calcium
- hyperoxaluria. Urinary oxalate is derived
primarily from endogenous hepatic production from metabolism of ascorbic
acid, glyoxylate, and glycine. A lesser amount of oxalate is derived
from the diet.
- reduction in crystal inhibiting agents.
In humans (& perhaps in dogs) inhibitors of calcium oxalate include
citrate, magnesium, pyrophosphate, glycosaminoglycans, nephrocalcin, and
Tamm-Horsfall mucoprotein
- Acidosis reduces the urinary excretion of citrate
which is a potent inhibitor of calcium oxalate
- Obesity is also a risk factor
- Dogs with hyperadrenocorticism have a predisposition to developing
calcium oxalate uroliths. Glucocorticoids increase the urinary excretion
of calcium.
Diagnostic information includes:
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monhydrate
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Calcium oxalate crystals may be observed in urine. They may be octahedral
shaped (dihydrate) or spindle shaped (monohydrate). Normal animals can have
a few oxalate crystals and not all animals with calcium oxalate uroliths
will have crystals in their urine.
Calculi are radiodense and can be observed on survey radiographs or with
ultrasound unless they are very small.
Treatment
Calcium oxalate uroliths must be surgically removed since attempts to
dissolve calcium oxalate uroliths in dogs have been unsuccessful.
Prevention
After removal
preventative measures against reoccurrence
should be initiated. Without preventative measures
recurrence rates are ~50 % within 3 years. Recommendations for
prevention, especially dietary recommendations are in flux
and you will find conflicting recommendations
in the literature.
Recommendations that are generally accepted:
- increase water intake by feeding canned food
and/or adding water to the food
- do not restrict P as P contributes to
pyrophosphate, a crystal inhibiting agent. Low P in the diet may
increased Ca uptake.
- avoid acidifiers which increase urine calcium excretion and decrease
urine citrate. Target urine pH of at least 6.5
to 7.0. This may be accomplished by some diets
or use of potassium citrate. Alkaline
urine enhances the tubular reabsorption of calcium.
Potassium citrate also inhibits calcium
oxalate crystal formation (is a crystal inhibitor).
- avoidance of oxalates from foods such as spinach, rhubarb and
parsley
- avoid vitamin C, which increases oxalate production
- avoid vitamin D which increases intestinal
absorption of calcium
Dietary recommendations
Previous recommendations to
reduce the risk of calcium oxalate urolithiasis included
reduced dietary levels of protein, sodium, and
calcium. Conversely, epidemiologic studies
published in 2002 cited reduced
risk of calcium oxalate urolithiasis with dietary
increases in protein, sodium and
calcium.
Calcium: increased or decreased?
It was previously
recommended to restrict dietary calcium which results in
reduction in urinary calcium. Recent
studies in people and dogs indicate that
restriction of dietary calcium increases the risk
as reduced dietary calcium increases the
dietary absorption of oxalate because less oxalate
is bound by calcium in the intestinal lumen; the
result is increased urinary oxalate excretion.
Although diets replete in calcium
are recommended, calcium supplements between meals should be avoided.
Sodium: increased or decreased?
Dietary sodium restriction has previously been recommended
as sodium excretion in the urine increases calcium
excretion. On the flip
side, the diuretic effect of increased dietary sodium
may reduce the urinary calcium concentration by
dilution which may reduce the risk of crystallization.
The commercial diets most often recommended include Waltham
Canine S/O Lower Urinary Tract Support Diet and Hill's
UD. UD has the disadvantage of being restricted in P. Hills WD
plus potassium citrate has also been recommended.
High fiber diets seem to decrease the degree of hypercalcemia in those
patients with elevated serum calcium.
Monitor
Monitor UA. Effective control should result in neutral to slightly
alkaline pH and absence of CaOx crystals. If crystals are
still observed then consider thiazide diuretics (hydrochlorothiazide)
which decrease urine calcium excretion. They
should be avoided in hypercalcemic states.
If pH is still acidic, consider potassium
citrate supplementation
Urate uroliths
Urate calculi form from uric acid which is the end product of purine
metabolism. Purines are components from the nuclei of cells.
Purines are converted to xanthines which are converted to uric acid which
is converted to allantoin. Allantoin is the substance which is excreted in
the urine in most dogs and cats.
The prevalence of urate
calculi is less than for struvite uroliths. Urate uroliths can be
comprised of 100% uric acid or a sodium or ammonium salt of uric acid. In
dogs, 90% of urate uroliths are ammonium urate. Urate uroliths may be mixed
with calculi of other mineral types.
Predisposing factors for development of urate uroliths include:
- enhanced uric acid excretion in urine
- acid urine pH
- absence of inhibitors of urolith formation
- elevated blood ammonia
Dalmatian dogs are homozygous for a recessive trait which predisposes
them to development of urate calculi. The defect results in impaired ability
of hepatocytes to take up uric acid. The hepatocytes are responsible for the
conversion of uric acid to allantoin. If the hepatocytes cannot take up uric
acid, the concentration of uric acid is increased in the blood.
Additionally, Dalmatians have impaired renal proximal tubular reabsorption
of uric acid leading to increased levels of uric acid in urine. It is
possible that non Dalmatian dogs which form urate uroliths are also
homozygous for this trait.
Patients with hepatic disease or portosystemic shunts have a reduced
ability to produce allantoin from uric acid with a resultant increase in
blood and urine uric acid concentration. Additionally patients with hepatic
disease have an impaired ability to convert ammonia to urea with resultant
hyperammonia.
Approximately 70% of dogs which develop urate uroliths are male. Breeds
which are particularly susceptible include the Dalmatian (60% of urate
stones occur in Dalmatians), bulldogs, and Yorkshire terriers. Urate calculi
are generally not associated with UTI. They appear as multiple small, round,
green-brown calculi.
If urethral calculi are present they should be hydropropulsed into the
bladder. Urate calculi can be surgically removed or dissolved. Medical
management includes:
- feeding a low protein/low purine diet which avoids lean meats and
glandular organs which are high in purines. UD diet by Hills is
9.5%-10.4% protein dry matter
- allopurinol which is a xanthine oxidase inhibitor is administered at
30 mg/kg/day divided BID or TID
- sodium bicarbonate or potassium citrate will reduce the renal
production of ammonia and should be dosed to a urine pH of 7.0 with 1/4
tsp/5 kg TID (sodium bicarbonate) as a starting dose. UD may maintain
alkaline urine without addition of an alkalinizing agent.
- Salt diuresis (1/4 tsp/5 kg daily) or mixing water with food will
dilute crystals
Medical therapy is continued therapy for at least 1 month following
radiographic disappearance of uroliths.
Recurrence is common with 33-50% recurrence within 1 year. UD may be fed
indefinitely to reduce recurrence. Other measures (alkalinizing agents,
allopurinol) may need to be introduced in a stepwise fashion if diet change
alone is insufficient to control recurrence.
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are caused by an inherited sex linked metabolic abnormality resulting in
tubular inability to reabsorb the amino acid, cystine and occasionally other
amino acids. The
prevalence is low
compared to other mineral types. Cystinuria may occur in both sexes but
cystine calculi occur more often in males. Not all dogs with cystinuria
develop urolithiasis. The calculi usually occur in younger animals, with a
mean age of 4.8 years. Dachshunds are the most common breed to develop
cystine uroliths.
Cystine uroliths are usually small, smooth, yellow brown to yellow green.
They can be radiopaque or radiolucent depending upon their size.
Cystinuria can be detected by identification of hexagonal cystine
crystals in acid urine or by performing a nitroprusside test on urine.
Cystine uroliths can be surgically removed or medically dissolved.
Medical management includes:
- feeding a protein restricted diet low in methionine such as UD
- increasing water intake will dilute the crystals but salt should not
be administered as increased sodium may increase urine cystine excretion
- increasing urine pH > 7.5 will increase solubility of crystals.
Potassium citrate is preferred over sodium bicarbonate due to sodium's
effect on increasing urine cystine.
- D-penicillamine changes cystine to more soluble form. It is dosed at
10-30 mg/Kg divided BID. One author suggests this dose to be intolerable
by many patients and advocates a dose of 10 mg/Kg. D-penicillamine
delays wound healing, so avoid use immediately postoperative if calculi
are surgically removed. Alpha-mercaptopropionylglycine (MPG) - has
fewer side effects which appears to be more effective than D-penicillamine
but is not approved yet for use in dogs. Dr. Osborne at the University
of Minnesota has had success in dissolving cystine calculi using Hills
UD and 2 MPG.
Avoid breeding affected animals due to the inherited nature of the
defect.
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are composed of amorphous silica. The
prevalence is low and German Shepherds may be over represented. Silica
uroliths occur frequently in dogs in Kenya as dog food is predominantly
corn. Dogs drinking from water sources containing sand may also develop
silica uroliths. Silica uroliths are shaped like a jack and are radiodense.
There are no characteristic crystals in the urine. Silica will not be
detected by calculi analysis using commercial kits (Oxford stone analysis
set - Oxford labs).
They must be surgically removed.
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Most nephroliths in dogs and cats are calcium oxalate or struvite, with
calcium oxalate being the most common.
Clinical signs are determined by:
- the size and rate of growth of nephroliths
- unilateral or bilateral involvement
- location (do the stones obstruct the ureters?)
- concomitant infection
- renal function prior to stone formation
Clinical signs may include:
- a symptomatic
- hematuria (microscopic or gross)
- signs of uremia and/or sepsis if pyelonephritis is present
- death from bilateral obstruction of renal pelves/ ureters
- unilateral obstruction causes unilateral hydronephrosis that may be
silent. if not associated with infection
Treatment
Not all animals with clinically silent nephroliths need to be treated.
Symptomatic and young animals should be considered candidates for treatment.
Treatment may be medical or surgical. Surgical removal of uroliths is
usually staged into 2 procedures, 4 to 6 weeks apart in animals with
bilateral stones. Nephrotomy was shown to cause a 20 to 40% reduction in GFR
in previously healthy dogs. The study only lasted 6 weeks so it is unknown
how much function may be regained. You might consider removing stones(s)
from one kidney and if the mineral analysis is struvite, attempting medical
dissolution of the stone(s) in the opposite kidney.
An alternative to surgery is the use of shock wave lithotripsy to break
stones into smaller pieces that can be passed. Although the technique is not
widely available for animal patients, it has been shown to be effective in
dogs with nephroliths. The use of lithotripsy requires the stone be in a
fixed position. Therefore lithotripsy is not very effective for bladder
stones although some veterinarians have used lithotripsy to break up large
stones in the bladder to hasten their dissolution by dietary means.
There is a fair amount of information on the use of lithotripsy for
fragmenting renal calculi in dogs and some recent information on the use of
lithotripsy in cats. Lithotripsy does cause some degree of renal trauma
resulting in renal swelling or hemorrhage and has been associated with
worsening of renal function in cats so the risks versus benefits need to be
weighed in this species.
Lithotripsy: an update on urologic applications in small animals.
Struvite nephroliths can be dissolved using an acidifying diet restricted
in protein, magnesium, phosphorus and high in salt, monitoring
as for dissolution of
bladder stones.
Method to prevent reoccurrence are the same as for struvite calculi in
the bladder.
Calcium oxalate calculi can not be dissolved. Management to prevent
reoccurrence of calcium oxalate nephroliths after surgical removal is the
same as for preventing bladder stones of the same mineral type.
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Dietary Manipulation
Given that several parameters that constitute risk factors for calcium
oxalate urolithiasis predispose to struvite urolithiasis and vice versa, pet
food companies have adopted one of 2 strategies:
1. separate diets designed to reduce the occurrence of each mineral type
2. a combined diet that results in a pH low enough to reduce struvite
urolith formation yet high enough to reduce calcium oxalate urolith
formation. These diets have varied degrees of mineral restriction and some
have potassium citrate added to increase the solubility of oxalate
crystals.
Also see
Nutrition Support
Service at Ohio State
Lower Urinary Tract Disease in
Veterinary Focus - Vol. 17(1) 2007 FREE access via
IVIS
International Veterinary Information Service
Hills Symposium on lower Urinary Tract Disease April 2007
Minnesota urolith center
Last Edited: Apr 30, 2008 4:45 PM
