Cats and Calcium Oxalate

Abstract

Practical relevance Calcium oxalate (CaOx) containing stones are among the most common of the urinary tract stones identified in cats.

Risk factors Risk factors for CaOx stone formation include such things as breed, gender and diet; stress and obesity have also been hypothesized to be risk factors for this disease.

Management approach A tailored, individual management strategy for preventing CaOx stone recurrence is important and should include addressing the diet, environment and any other comorbid conditions present. Increasing the cat's moisture intake is one of the key mechanisms for preventing recurrence.

Clinical challenges CaOx ureterolithiasis has emerged as a difficult and sometimes life-threatening problem for cats. In those cats where stones are found incidentally, periodic monitoring may be required to assess for disease progression. Interventional procedures such as ureteral stent placements are now increasingly being performed for recurrent cases or those with larger stone burdens. Periodic radiographs for more severe cases and frequent client communication can help ensure successful outcomes for cats with lower and upper CaOx stone disease.

Evidence base Limited evidence-based studies are published regarding management of feline upper and lower urinary tract CaOx stone disease, making this a difficult condition to manage in some cats. Studies designed to evaluate the relationship to dietary modifications, medical management, stress, obesity and surgical techniques are warranted in cats with upper and lower urinary tract CaOx stones.

Feline urinary tract stone disease

Epidemiological trends

The two most common feline urinary stones (calculi) submitted for analysis are calcium oxalate (CaOx) and struvite. It is difficult to discuss trends in CaOx formation without discussing struvite alterations as well. Their relative frequencies of submission to stone analysis laboratories have changed over the years.

In 2007 we reported that CaOx was the most common mineral type found in submissions to the GV Ling Urinary Stone Analysis Laboratory at the University of California, Davis.¹ Struvite containing stones significantly decreased during the 1990s (Fig 1).¹ Based on previously published epidemiological studies, struvite was the most common stone reported in cats until approximately 1993, when the incidence of CaOx began to increase; at that point 53% of stones contained CaOx, and 47% contained struvite.¹ Other stone laboratories have reported similar findings.^2,3

The concern regarding struvite stone disease in cats seemed to have led pet food manufacturers to restrict the magnesium content of feline diets and also resulted in the formulation of diets with greater urinary acidifying potential. Unfortunately, an increase in the frequency of CaOx stone disease appears to have occurred since these dietary modifications began. Although dietary acidification can enhance the solubility of struvite crystals in the urine of cats, it also promotes the release of calcium carbonate from bone as a metabolic buffer, resulting in hypercalciuria.⁴ Results have shown that differences in age, sex, breed and reproductive status did not contribute to the apparent reciprocal relationship between occurrences of CaOx and struvite stones in cats.² Submissions of stones not containing CaOx or struvite appeared to be static during that same time period.

An increase in the frequency of CaOx stone disease appears to have occurred since dietary modifications were introduced to address struvite stones in cats.

MULTIMEDIA

A video recording of ureteral stent placement for treatment of ureterolithiasis is included in the online version of this article at 10.1016/j.jfms.2011.07.018

More recently still, the trends in struvite and CaOx stone submission to the authors’ laboratory have changed. Based on analyses in the past 5 or so years, the proportion of struvite stones and CaOx stones submitted to our laboratory appears to be similar (Fig 1). One possible explanation for this could be that highly acidifying diets are being prescribed less commonly, but dietary histories have not been available from the clinical records to confirm or deny this hypothesis.

FIG 1

Percentage of calcium oxalate (CaOx) and struvite containing stones among submissions to the authors’ laboratory. Note that the relative proportions of CaOx and struvite containing stones have changed significantly over time

It also must be recognized that, for a variety of reasons, the distribution of stones submitted for analysis may not accurately represent the distribution in the feline population.⁵

Where do CaOx stones occur?

CaOx stones can occur anywhere in the urinary tract. Approximately 73% of CaOx stones the authors analyzed from cats were removed from the bladder, 7.3% were removed from the ureter(s), 4.3% were removed from the kidney(s) and 13% were removed from the urethra; 2% were voided. Most cats having CaOx stones removed from the urethra or voided also had stones located elsewhere in the urinary tract.¹

Risk factors

Breed Several breeds have been reported to be at higher risk for struvite and CaOx stone disease. Evaluation of breed predispositions revealed that domestic longhair cats, Persians and Himalayan (Colourpoint Persian) cats had significantly more CaOx containing stones.¹ When evaluating recurrent CaOx urolithiasis in cats, a retrospective case control study of 2393 cats with CaOx uroliths reported that 6.8% had another CaOx stone submitted for laboratory analysis within a 2-year period.⁶

Age Cats ≥7 years but ≤10 years of age are reported to be 67 times more likely to develop CaOx uroliths than are cats between 1 and 2 years of age.²

Gender An increase in CaOx containing uroliths was detected in male cats, as compared with female cats,¹ while neutered cats were seven times more likely to develop CaOx uroliths as compared with sexually intact cats.²

Environment Stressful life events¹² and obesity^11,13 have been associated with more clinical events of urinary stone disease in humans. Studies investigating body mass index, body weight and environmental stressors, and urinary stone disease are warranted in feline patients to see what, if any, relationships exist.

Pathophysiology of CaOx stone formation

The exact mechanism of CaOx stone formation is unknown and likely involves interrelationships between gender, genetic (breed, familial), dietary and environmental factors. In cats with proven or suspected CaOx stone disease, serum should be evaluated to assess calcium levels. Elevated circulating calcium from various causes (neoplastic, primary or secondary hyperparathyroidism, or idiopathic hypercalcemia) can also predispose the cat to CaOx stone formation.

There is limited published information regarding the pathophysiology of stone formation in the cat. In humans, approximately 75% of kidney stones are composed predominantly of CaOx, and oxalate metabolism is thought to play a crucial role in stone development. Hyperoxaluria can occur from increased dietary intake as well as a loss or diminished activity of oxalate-degrading bacteria in the colon (Oxalobacter formigenes).⁷ Although urinary supersaturation with crystals is implicated in stone formation in humans, several studies have investigated the possibility that the urine is not the initial site of stone development. A vascular etiology for nephrolithiasis in humans has been proposed,⁸ suggesting that vascular abnormalities (eg, hypertensive vascular injury, atherosclerosis) can lead to Randall's plaques. These plaques are papillary lesions that are usually associated with calcium and phosphate or CaOx which shed into the urinary system.⁹ Stoller et al hypothesized that the primary event in CaOx nephrolithiasis in humans may begin in the vascular bed at the tip of the renal papilla.⁸

Several studies have investigated the possibility that the urine is not the initial site of stone development.

Therefore, the primary site of stone formation may be unrelated to urinary stasis, infection or other secondary causes for urinary stones and novel treatment regimens may need to be investigated. Still other studies have investigated a role for elevated lipids in CaOx stone formation in rats and in humans.¹⁰ An association between obesity,^11,13 stress¹² and CaOx stone formation has also been reported in humans, and it is unknown if this association occurs in cats.

Lower tract CaOx stones

Clinical signs

Cats with cystic calculi can present with lower urinary tract signs such as pollakiuria, stranguria, hematuria, periuria, or a combination of these. Male cats can also present with urethral obstruction secondary to a stone lodged in the narrow distal urethra. These clinical signs are not specific for urinary stone disease and other differentials such as feline idiopathic cystitis, urinary tract infections and neoplasia should also be considered when these signs are present. It is additionally important to note that bladder stones can be found incidentally and the cat may not have any clinical signs.

Diagnostics

CaOx stones are radiodense and can usually be easily seen on plain abdominal radiographs. When obtaining abdominal images, it is imperative that the entire urinary tract is included, especially the urethra in male cats, so as not to miss any stones that may be present (Fig 2). Oftentimes, radiography is all that is required to diagnose cystic calculi; however, ultrasound can also be used and will detect very small stones in the bladder as well as bladder sediment that can be missed on radiographs. The urethra cannot be imaged well using ultrasound though, and radiography and ultrasound should be used as complementary diagnostics.

FIG 2

Lateral abdominal radiograph of a cat that presented to the authors' clinic for recurrent lower urinary tract signs including intermittent stranguria and pollakiuria. This cat had six ultrasound examinations performed before a radiograph was obtained which identified a urolith in the distal penis. The stone (calcium oxalate) was removed surgically and the cat recovered uneventfully

Urinalysis should be performed in a cat with cystic calculi. Ideally, urine should be evaluated within 60 mins of collection to minimize time and temperature effects on in vitro crystal formation.¹⁴ The urine specific gravity should be recorded and reasonable goals to decrease this value can be established after stone removal. The urine pH in cats with CaOx is variable and CaOx crystals are not always present in cats with CaOx containing stones.

Management approaches

CaOx occurs in two common forms, CaOx monohydrate (whewellite) and CaOx dihydrate (weddellite) (Fig 3). Management approaches for the two different forms are the same.

FIG 3

(a) CaOx monohydrate stones removed from the bladder of a cat. Oftentimes, this form of CaOx is smooth and round. (b) CaOx dihydrate stones removed from the bladder of a cat. This form of CaOx can have small projections, as pictured here

Cats that have had prior cystic calculi should be monitored with radiographs every 2–3 months to assess for recurrence, and this time frame can be adjusted as the clinician evaluates the propensity for the cat to form more stones. If ‘sand and debris’ or even very small stones (2–3 mm in some female cats) are seen in the urinary bladder, surgery is often-times not necessary, and voiding urohydropropulsion may be used to remove the stones.¹⁵ In addition to radiographs, urinalyses should be monitored to ensure an appropriate urine specific gravity and lack of urine sediment. More detailed recommendations for monitoring cats with CaOx stone disease are given on page 654.

There is no dissolution protocol for CaOx stones, so removal and quantitative mineral analysis of the stones should be performed if they are growing or causing clinical disease. Animal-related factors should be addressed initially to ascertain that there are no intrinsic predisposing problems. If serum calcium concentration is elevated, a search should be initiated for underlying causes.¹⁶ A baseline urinalysis and urine culture should be performed, paying special attention to evaluation of urine specific gravity and urine sediment.

Dietary manipulations

Increasing the water consumption is the cornerstone of therapy for stone disease in human¹⁷ and veterinary medicine. In cats, this can be achieved most easily by feeding a canned diet. Gradual introduction of the high moisture diet may avoid a short initial period of diarrhea.

Voiding urohydropropulsion

The cat should be anesthetized to relax the urethra, prevent urethral spasms and allow easy bladder expression. A urinary catheter is inserted into the bladder and the bladder is distended with sterile saline. The bladder should feel full, but not so taut that bladder rupture could occur. With the catheter still in place, the cat should be held upright so that stones can fall into the trigone. As the catheter is removed, the clinician should express the bladder to create a forceful stream and collect the contents that are voided. When expressing the bladder, the palm of the hand (not the fingertips) should be used to help prevent trauma to the bladder. Several voids may be required to remove all the stones and stone debris present. Hematuria can result from this procedure, but usually resolves within 24 h.

Management recommendations for lower tract CaOx stones

Alternatively, if the pet will not consume a canned diet, water can be added to the dry kibble, although 85% moisture content (typical of feline canned diets) is difficult to attain using this method. If the cat does not accept and tolerate an increase in dietary moisture content, attempts can be made to increase voluntary water intake by using drinking fountains, and by adding flavored (ham, tuna) juices or ice cubes to the drinking water. Urine specific gravity should be monitored at periodic reevaluations to assess the adequacy of the current strategy. Urine specific gravity should be evaluated from samples obtained at home to gain a better understanding of owner compliance and water intake in the home environ-ment. A specific gravity of <1.025 for cats seems reasonable in the authors’ experience.

Several commercially available therapeutic diets are marketed as assisting to reduce the recurrence of CaOx stones in cats. A diet that is restricted in both calcium and oxalate seems logical for cats prone to urinary stone disease, but, to our knowledge, no evidence-based studies in cats with naturally occurring disease are available to support or refute the marketing claims. Reducing the dietary content of only one of the CaOx precursors could potentially increase the intestinal absorption and urinary excretion of the other. As with excess calcium, foods rich in oxalate or oxalate precursors should also be avoided. Future research for CaOx stone prevention in cats could focus on understanding oxalate metabolism, and dietary oxalate intake and absorption in cats.¹⁸

Other nutrients to consider in the dietary management of CaOx stones include magnesium and phosphorus. Urinary magnesium and phosphate (and citrate) are thought to act as inhibitors of CaOx stone formation and, therefore, should not be restricted in the diet. Dietary phosphorus should also not be excessively restricted because reduced serum phosphorus could result in increased activation of vitamin D₃ to calcitriol by 1-α-hydroxylase in the kidney, under the action of parathyroid hormone, and result in increased intestinal absorption of calcium.¹⁹ Lastly, as mentioned above, dietary fats have been speculated to be involved in CaOx stone formation in rats and in humans. Although the pathogenesis of CaOx stone formation in cats may differ, it may be prudent to feed obese cats a high moisture diet that is restricted in fat (less than 2 g/100 kcal diet) and/or calories.

Urine specific gravity should be evaluated from samples obtained at home to gain a better understanding of owner compliance and water intake in the home environment.

To salt or not to salt?

If, having utilized strategies to increase the moisture content of the diet, the urine is still too concentrated, and/or the urine sediment findings remain abnormal, one can try the addition of sodium chloride (table salt) to the diet to increase the urine volume produced daily.

According to the 2006 National Research Council publication, ‘Nutrient Requirements of Dogs and Cats', the upper safe limit of normal sodium intake by cats with free access to water has not been determined, but is greater than 15 g/kg diet, or about 40 g of salt. Most commercial diets contain less than 1% salt, so cautious addition of a few hundred milligrams per day (1/8 teaspoon of table salt weighs ~300 mg) should not be dangerous in otherwise healthy cats with free access to water.

Current recommendations for appropriate salt intake in animals with prior CaOx stones are controversial, but sodium chloride supplementation has been reported to increase urinary calcium excretion and increase the risk for CaOx stones in humans.²⁰ In dogs, calcium excretion was increased when consuming a higher sodium diet; however, the urine calcium concentration and relative supersaturation for CaOx was decreased.²¹ Similar studies have not been performed in cats. Dietary salt supplementation is not recommended for cats with reduced renal function, cardiac disease or hypertension.

No adverse effects of added sodium chloride have been noted in short-term published studies and abstracts in healthy cats ingesting diets containing up to 1.1–1.3% sodium on a dry matter basis.^22–24

Drug therapy

If dietary manipulations alone are unsuccessful in preventing CaOx stone recurrence, drug therapy may provide additional benefit.

Potassium citrate Administration of citrate as potassium citrate (Urocit-K, Mission Pharmacal; Polycitra liquid, Willen) could be helpful because urinary citrate may act as an inhibitor of CaOx stone formation. The liquid may be easier for cats, but the bitter taste can make medicating a cat difficult in some circumstances. Hypocitraturia may be a risk factor for CaOx stone formation in humans because citrate can become chelated to calcium, forming a more soluble salt than CaOx in the urine. This additive appears beneficial only to humans whose citrate excretion is low. The recommended dosage of potassium citrate is 100–150 mg/kg/day for cats, but it is unclear if this dosage will actually increase urinary citrate excretion in cats. In one study, urine citrate concentrations were only 1 μM, or less than ~20 μg/day.²⁵ This study suggests that urine citrate concentrations are low in the cat, but what, if any, benefit citrate supplementation has is yet to be determined.

Hydrochlorothiazide Hydrochlorothiazide is a diuretic that decreases urine calcium excretion in humans, and has been recommended to prevent recurrence of CaOx stone disease in dogs and cats. One study in dogs reported that hydrochlorothiazide significantly reduced urine calcium excretion.²⁶ The hypocalciuric effect of this drug may be negated by augmentation of oral fluid intake. When evaluating the effects of hydrochlorothiazide and calcium excretion in healthy cats, a decrease in the relative supersaturation for CaOx was reported, but no changes in 24 h urinary calcium or citrate excretion were found.²⁷ No adverse side effects were noted at a dose of 1 mg/kg q12h. The administration of hydrochlorothiazide is contraindicated in cats with hypercalcemia.

Upper tract CaOx stones

Epidemiology

Ureterolithiasis has emerged as an important cause of acute and chronic kidney disease in cats over the past 15 years. In a study by Kyles et al, it was reported that 98% of feline ureteroliths contained CaOx.²⁸ Most stones submitted from the upper urinary tract of cats are comprised of 100% CaOx, although occasionally calcium phosphate (in the form of apatite) or urate are present in the layers of the CaOx stones.²⁹ Ureteral stone submissions have increased significantly over the past 15 years.^1,30 Although ureteroliths account for only 2% of the total number of feline stones submitted to the authors’ laboratory, there has been a significant increase in the proportion of CaOx containing ureteroliths submitted over time.¹ The authors now do not see struvite in the upper urinary tract of cats and this change in stone composition may be partially associated with changes in feline diets that were described earlier. However, the emergence of ureterolithiasis may be associated with an increased prevalence of CaOx urolithiasis in cats, an increased awareness of ureterolithiasis, and/or an increased use of diagnostic imaging in cats with renal disease.

Although reported less often, other causes of ureteral obstruction can include soft tissue plugs (which sometimes contain flakes of mineralized material), inflammatory ‘debris’ in cats with pyelonephritis, and calculi that are comprised of 100% dried solidified blood.³¹ A healthy feline ureter has a luminal diameter of approximately 0.4 mm; this is roughly equivalent to the diameter of 2-0 suture.³² In patients with a chronic stone burden, where stones have passed previously, significant ureteral inflammation and/or stricture can develop, further decreasing the luminal diameter through which material can pass. This can lead to an even higher risk for development of ureteral obstruction with minerals, and debris that would pass in a normal ureter leads to obstruction in the more compromised ureter.

Signalment

While cats as young as 8 months have been diagnosed with ureteral stones, ureterolithiasis tends to develop in middle-aged to older cats, with a median age of 7 years at the time of diagnosis.²⁹ No studies have documented a definitive gender predilection for ureteral obstructions, but CaOx stones in general are reported more often in male cats.¹

Clinical signs

The clinical signs associated with ureterolithiasis are variable and are often related to the rate at which ureteral obstruction develops; patients with acute obstruction and rapid renal capsular distension are often more painful as compared with patients with more insidious obstructions.³³ Non-specific signs can include reduced appetite, weight loss, lethargy and hiding. Cats may also present with hematuria without concurrent lower urinary tract signs such as stranguria, pollakiuria and dysuria. When hematuria alone is noted in a cat without concurrent lower urinary tract signs, evaluation for CaOx containing upper tract stones is warranted. Depending on the degree of renal compromise, either pre-existing before obstruction or secondary to obstruction, many cats will have clinical signs associated with azotemia. While some feline patients do not appear to be in pain, humans report significant discomfort associated with ureteral obstruction and it is the experience of the authors that many feline patients do exhibit signs of pain in association with ureteral obstruction; it is, therefore, critical to evaluate an affected cat for pain and to treat when appropriate.

When hematuria alone is noted in a cat without concurrent lower urinary tract signs, evaluation for CaOx containing upper tract stones is warranted.

Some cats with ureteral obstruction may not exhibit any clinical signs and, therefore, it is possible to diagnose a chronic ureteral obstruction as an incidental finding. One example of this is the ‘big kidney, little kidney syndrome’ (Fig 4). This is a phrase that is used to describe cats that have one non-functional or minimally functional kidney due to a previous ureteral obstruction, which then develop an acute ureteral obstruction in the remaining and functional kidney, which can enlarge. The functional kidney may also enlarge secondarily to compensatory hypertrophy over time. In many cases, the initial obstructing event goes unnoticed by the owner, as clinical signs are not evident until the cat develops significant azotemia associated with bilateral ureteral obstruction.

FIG 4

Lateral abdominal radiograph of a cat with ‘big kidney, little kidney syndrome'. It is theorized that cats with this problem have had a prior ureteral obstruction, and one kidney has atrophied and lost function. The other kidney can enlarge secondarily to compensatory hypertrophy over time, or due to another acute obstruction. In many cases, the initial obstructing event goes unnoticed by the owner, as clinical signs are not evident until the cat develops significant azotemia from the second obstructive event

Diagnostics

Diagnostic imaging of the abdomen should be performed in all cats with azotemia. CaOx containing stones are radiopaque and, if present, are often seen on plain abdominal radiographs (Fig 5). The sensitivity of survey abdominal radiography for the diagnosis of ureterolithiasis is 81%.²⁹ CaOx containing ureteral stones are most readily identified in the retroperitoneal area on a lateral radiographic projection; however, it can be difficult to determine from lateral radiographs alone which ureter is involved or whether one or both ureters are affected. The radiographic identification of mineralization in the region of the ureters may not define the true location of the obstruction, or may identify only one area of obstruction, when multiple may be present. Small stones, stones overlying the colonic contents, and radiolucent calculi or obstructive debris may be missed on survey radiographs.

FIG 5

Lateral abdominal radiograph in a cat revealing multiple radiodense opacities within the renal pelvis and retroperitoneal space where the ureters are located. These are highly suggestive of CaOx stones within the kidneys and ureters

Abdominal ultrasound is a complementary imaging study for cats suspected of having ureteroliths. The sensitivity of abdominal ultrasonography for the diagnosis of ureteral calculi is 77%. While this is lower than plain radiography, ultrasound images can help delineate which ureter is obstructed, and the severity of hydronephrosis and hydroureter that may be present. A combination of survey radiography and ultrasonography is recommended and has a sensitivity of 90% for the diagnosis of ureterolithiasis.²⁹

The hydroureter often does not extend to the level of the obstructing ureteral stone and this may explain why ultrasound examination can sometimes fail to identify a stone. In one study in which 155 cats with ureteral obstruction underwent surgery, dilation of the ureter and/or renal pelvis was observed ultrasono-graphically in 143 (92%) cats, was equivocal in three cats and was absent in nine cats.²⁹ In subacute ureteral obstructions, ureteral and pelvic dilation may have not yet developed, so it is critical to consider ureteral obstruction as a differential in appropriate cases, even when dilation is not present.³³

A combination of survey radiography and ultrasonography has a sensitivity of 90% for the diagnosis of ureterolithiasis.

Additional imaging modalities, such as antegrade pyelography or computed tomography, may be necessary to identify calculi that are not apparent on survey radiography or ultrasonography.

Management approaches

Conservative medical management

There is no dissolution protocol for upper tract CaOx containing stones. Conservative medical management for cats with minimal or no renal compromise can be effective. While there are no studies in cats to evaluate the efficacy of any of the treatments mentioned, most experienced clinicians will agree that expulsive therapy may play a role in the management of this disease in stable patients. Suggested therapies include intravenous fluid diuresis with administration of the diuretic, mannitol, with or without other drug therapies.

In humans with ureterolithiasis, the α-adrenergic antagonist, tamsulosin, is often used and favorable outcomes have been reported, particularly when stones are in the distal third of the ureter.³⁴ This and other α-antagonists such as phenoxybenzamine and prazosin have been anecdotally used in cats, with variable responses. In one report, amitriptyline, a tricyclic antidepressant, was shown to facilitate passage of urethral plugs in cats; further studies evaluating ureteral tissue from rats, pigs and humans found amitriptyline to inhibit smooth muscle contractions, suggesting it might be a useful therapy for ureteral obstruction in cats.³⁵ While no studies have evaluated the efficacy of any of these drugs, the authors often use prazosin (typically in combination with mannitol), given its relatively low cost and its more rapid time to achieve therapeutic levels. Pain management with drugs such as buprenorphine should also be used to prevent ureteral spasm, which could prevent ureterolith movement.

Conservative medical management for cats with upper tract CaOx containing stones, but minimal or no renal compromise, can be effective.

If azotemia or pyelonephritis is present, surgery, or other newer minimally invasive techniques (eg, ureteral stents) for restoration of urine flow, should be considered.

During conservative management it is crucial to critically evaluate patient stability and fluid status. Cats should be monitored by serial measurements of serum creatinine and blood urea nitrogen concentrations, and these are often the most sensitive indicators that the obstruction has improved or progressed. It is important to remember that if significant intrinisic renal damage has occurred, passage of a ureteral obstruction does not always lead to immediate improvement in azotemia; rarely, in cases with significant kidney disease prior to obstruction, severe azotemia may persist. Serial radiography and ultrasonography can be useful in monitoring the success of medical management for ureterolithiasis. It has also been reported that stones can spontaneously move retro-gradely back into the renal pelvis rather than passing into the urinary bladder.³⁶

In cats treated medically that survived >1 month after diagnosis, the 12-month survival rate was 66%, with a number of cats dying of causes related to chronic kidney disease or recurrent ureterolithiasis. When a subset of cats were followed, a 40% recurrence rate was documented if uroliths were present in either renal pelvis.³⁷ Cats with significant elevations in serum potassium or fluid overload at the time of initial examination may benefit from aggressive medical management such as hemodialysis (Fig 6). Oftentimes, impaction of the stones in the ureteral mucosa impairs their passage to the bladder.

FIG 6

An 11-year-old male castrated Abyssinian undergoing hemodialysis treatment for ‘acute on chronic’ kidney disease

If azotemia or pyelonephritis is present, surgery, or other newer minimally invasive techniques (eg, ureteral stents) for restoration of urine flow, should be considered.

Ureteral stents

Placement of ureteral stents can be performed for treatment of feline ureteral obstruction, particularly for those cats with multiple ureteroliths, previous ureteral obstruction or concurrent renoliths. Long-term outcome data regarding use of ureteral stents in cats is lacking; however, the subjective experience of the authors is positive.

Attempts to place stents using a retrograde endoscopic approach have been made, but have been largely unsuccessful in cats. A relatively minimally invasive surgical placement is used, whereby the surgeon performs a laparotomy and places the stent from the kidney and into the bladder using a coaxial technique. In most cases, a needle puncture in the kidney and cystotomy are the only incisions that are made in the urinary system. After initial placement, urine should flow through the stent lumen and, over time, ureteral dilation develops around the stent passively, allowing further passage of urine, crystals and possibly stones around the stent.

Stents are typically left in place long term, unless this becomes contraindicated due to infection or patient discomfort.

Surgical intervention

While the optimal time for medical management before making a decision to pursue surgery has not been determined in cats, and the improvement in renal function after stone removal is variable, early surgical intervention is likely indicated in an effort to maintain a functional kidney. Surgical removal of ureteral stones should be considered when there is evidence of partial or complete ureteral obstruction. The number of stones, degree of obstruction, surgeon experience and availability of appropriate equipment should all be considered when making decisions to proceed with ureterotomy.

Major factors determining the recovery of renal function after re-establishing ureteral patency include renal function prior to development of obstruction, and the duration and extent of the obstruction. Ureteral strictures secondary to scar tissue formation can also form at the ureterotomy site, leading to re-obstruction; these complications are much less likely to occur when ureteral stenting is performed (see box).

Long-term strategies

Because of the possibility of recurrence of CaOx stones, long-term management strategies should be implemented, as appropriate. Similar to lower urinary tract CaOx stone disease, if the serum calcium level is elevated, a search for an underlying cause should be performed and appropriate therapy should be prescribed as indicated. In cats with chronic kidney disease, appropriate medical and dietary management should be instituted. Diets should be high in moisture and feeding tubes can be used, especially in the postoperative period, to ensure adequate caloric and water intake. If cats are azotemic, the authors often prescribe prescription canned renal diets with added water for management.

Hydrochlorothiazide and potassium citrate can be added to the management protocol, particularly for recurrent cases. Hydrochlorothiazide can cause gastrointestinal upset in cats, particularly those that are azotemic; this drug should not be used in moderate to severely azotemic cats. If concurrent aluminum-containing phosphate binders or antacids are being administered, potassium citrate should not be used as aluminum toxicity and metabolic alkalosis, respectively, can occur.³⁸

Case notes

Stella, a 7-year-old female spayed domestic shorthair cat, presented with oliguria/anuria and a decreased appetite.

Pertinent history Stella previously presented for anuric renal failure (BUN 184 mg/dl [65.7 mmol/l], reference interval [RI] 18–33 mg/dl [6.4–11.8 mmol/l]; creatinine 16.8 mg/dl [1485.1 μmol/l], RI 1.1–2.2 mg/dl [97.2–194.5 μmol/l]) due to presumed lily intoxication given recent exposure to a lily plant. At that time, abdominal ultrasound revealed no visible left kidney (suspected left renal agenesis) and non-specific changes suggestive of nephritis in the right kidney. No signs of ureteral obstruction were noted. She was treated with hemodialysis and improved in 5 days.

Given this rapid recovery, lily intoxication was considered unlikely, as patients with lily intoxication typically take several weeks to regain renal function, if at all. Ureteral obstruction was suspected despite the lack of urinary tract distension on initial imaging studies. Urinary tract dilation is not always present in acute forms of ureteral obstruction.

Stella was referred to the authors’ clinic again 1 year later with suspected anuric renal failure diagnosed by the referring veterinarian. On physical examination, she was quiet but responsive and euhydrated. A firm and enlarged right kidney was palpable and Stella resented abdominal palpation. The BUN was 154 mg/dl (55.0 mmol/l) and creatinine was 14.9 mg/dl (1317.2 μmol/l). Abdominal ultrasound at this time revealed significant renal pelvic and ureteral dilation (see left); ureteral obstruction was suspected. Ultrasound did not reveal a discrete stone obstructing the ureter, but rather small mineral material with cellular debris. Due to the radiodense material present within the ureter, an obstruction with CaOx was suspected.

Ultrasound image of Stella's right kidney. Note the significant pelvic dilation (hydronephrosis), which is present secondarily to a complete ureteral obstruction. Despite dilation of the renal pelvis, there is still a substantial amount of parenchmyal tissue present, suggesting that renal function may return once the obstruction is resolved

Aggressive medical management was instituted, including hemodialysis for initial stabilization. Mannitol (0.5 g/kg IV slowly q8h) was given as an osmotic diuretic to increase urine flow and to help promote diuresis and possible stone migration down the ureter. Prazosin (0.5 mg PO q12h) and buprenorphine (0.01 mg/kg IV q6h) was also used to help decrease ureteral spasm, thereby aiding movement of the obstructive material down the ureter. Antibiotics (ampicillin 20 mg/kg IV q8h and enrofloxacin 2.5 mg/kg IV q24h) were used prophylactically in case pyelonephritis was present; due to anuria, a urine culture could not be obtained. On the fifth day of hospitalization, Stella passed the ureteral obstruction, became polyuric and the azotemia resolved. She was maintained on canned food (Royal Canin LP) with added water.

Three months later, Stella had presented again for a suspected ureteral obstruction.

Examination findings On physical examination an enlarged and painful right kidney was present; a left kidney was not palpable. Abdominal ultrasound revealed an enlarged right kidney with significant renal pelvic and proximal ureteral dilation. There was a mild amount of retroperitoneal fluid and the urinary bladder was empty. The remainder of the examination was within normal limits. BUN was 178 mg/dl (63.5 mmol/l) and creatinine was 14.1 mg/dl (1246.4 μmol/l).

Treatment plan Stella was stable and did not require dialysis at the time of presentation. She was treated with conservative intravenous fluid diuresis (0.9% sodium chloride) to maintain hydration but prevent fluid overload. Mannitol and prazosin were administered as previously described. Due to the propensity for Stella to form small presumed CaOx concretions that cause ureteral obstruction, ureteral stent placement was planned.

The stent was placed without complication (see radiograph).

Dorsoventral abdominal radiograph after ureteral stent placement for treatment of obstruction. The double pigtail stent can be visualized curled within the renal pelvis, tracing down the ureter and forming the second pigtail within the urinary bladder

Clinical outcome Stella remained oliguric for 24 h after surgery, likely due to acute kidney injury that developed secondarily to obstruction; however, she became significantly polyuric at 24 h. Azotemia resolved 72 h later and, at the time of writing 9 months post-stent placement, Stella had remained non-azotemic.

Footnotes

Acknowledgements

The authors are grateful to Dr Bill Culp, of UC Davis School of Veterinary Medicine, for providing the accompanying video footage of ureteral stent placement.

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