Some mineral solutes precipitate to form crystals in urine; these crystals may aggregate and grow to macroscopic size, at which time they are known as uroliths (calculi or stones). Uroliths generally contain an organic matrix that is believed to vary minimally among uroliths and that constitutes ~2%–10% of the stone’s chemical composition. The remaining 90%–98% of the urolith is composed of minerals that vary depending on the type of urolith. Urolithiasis is a general term referring to stones located anywhere within the urinary tract. Uroliths can develop in the kidney, ureter, bladder, or urethra and are referred to as nephroliths, ureteroliths, urocystoliths, and urethroliths, respectively.
Uroliths in all animal species are composed of ~10 different minerals. Identification of the minerals in uroliths by qualitative analysis is unreliable. The type of minerals in uroliths can be readily identified by optical crystallography, infrared spectroscopy, and/or x-ray diffraction. Minerals found in uroliths have a chemical name and often a mineral or crystal name (see Table: Urolith Names). Variation in urine characteristics over time can result in more than one crystal type within a single urolith. In such instances, the urolith core corresponds to conditions that were present when the urolith initially formed, and the outer layers correspond to more recent conditions.
Mechanisms involved in stone formation are incompletely understood in dogs and cats. However, three main contributing factors are 1) matrix—the inorganic protein core may facilitate initial urolith formation, 2) crystallization inhibitors—organic and inorganic crystallization inhibitors may be lacking or dysfunctional in animals with uroliths, and 3) precipitation crystallization factors—a complex relationship among urine solutes and other chemical factors in the urine can lead to conditions favoring crystallization. Regardless of the underlying mechanism(s), uroliths are not produced unless sufficiently high urine concentrations of urolith-forming constituents exist and transit time of crystals within the urinary tract is prolonged. For selected stones (eg, struvite, cystine, urate), other favorable conditions (eg, proper pH) for crystallization must also exist. These criteria can be affected by urinary tract infection, diet, intestinal absorption, urine volume, frequency of urination, therapeutic agents, and genetics.
Clinical signs associated with urolithiasis are seldom caused by microscopic crystals. However, formation of macroscopic uroliths in the lower urinary tract that interfere with the flow of urine and/or irritate the mucosal surface often results in dysuria, hematuria, and stranguria. Nephroliths often are asymptomatic unless pyelonephritis exists concurrently or they pass into the ureter. Ureteral obstruction may produce signs of vomiting, lethargy, and/or flank and renal pain, particularly if there is acute total obstruction with distention of the renal capsule. The only clinical sign associated with unilateral urethroliths may be pain, which can be difficult to detect in dogs and cats. If these initial signs of ureteral obstruction do not lead to a diagnosis, unilateral ureteral obstruction may result in hydronephrosis with loss of function of the ipsilateral kidney. Ureteroliths may also precipitate a uremic crisis in cats with previously compensated chronic renal failure. Because clinical signs of renal dysfunction are generally not apparent until two-thirds or more of total functional renal parenchyma is lost, clinical signs may not be seen except in the following situations: 1) both ureters are obstructed, 2) there is contralateral chronic kidney disease, or 3) a renal infection develops. Unilateral ureteroliths may be identified serendipitously during abdominal imaging studies or surgery.
Abdominal palpation can help detect urocystoliths; the bladder wall may be thickened, and a grating sensation may be felt when the bladder is palpated. Although palpation may reveal a single large urolith or multiple uroliths by their crepitation, it cannot dependably identify all animals with uroliths; urethral calculi may be detected by rectal palpation or located by passing a catheter. Because multiple uroliths may be present throughout the urinary tract, a complete radiographic examination of the tract is indicated; radiodense calculi >3 mm in diameter are usually visible on radiographs. Urate, and occasionally cystine, uroliths may be radiolucent, requiring contrast radiography or ultrasonography to confirm their presence. Urinalysis, including identification of crystals on microscopic examination of fresh, warm urine and bacterial culture and sensitivity testing, is a critical part of the evaluation and may help determine the type of urolith present. Ultrasonography and cystoscopy may also be useful.
Urethral obstruction is common in male dogs and cats. It may occur suddenly or may develop throughout days or weeks. Initially, the animal may frequently attempt to urinate and produce only a fine stream, a few drops, or nothing. Animals may also exhibit extreme pain manifested by crying out when attempting to urinate. Complete obstruction causes uremia within 36–48 hr, which leads to depression, anorexia, vomiting, diarrhea, dehydration, coma, and death within ~72 hr. Urethral obstruction is an emergency condition, and treatment should begin immediately.
If the bladder is intact, it is distended, hard, and painful; care should be used when palpating the bladder to avoid iatrogenic rupture. If the bladder has ruptured, it cannot be palpated and urine can sometimes, but not always, be obtained from the abdominal cavity by paracentesis. Animals with spontaneous bladder rupture may appear temporarily improved because the pain associated with bladder distention has been relieved; however, peritonitis and absorption of uremic toxins and potassium occur rapidly and lead to depression, abdominal distention, cardiac arrhythmias, and death.
Hyperkalemia and metabolic acidosis are life-threatening complications of urethral obstruction. An ECG (to record cardiac rhythm and rate) and a serum potassium are indicated. Initial emergency care involves immediate relief of obstruction by catheterization and fluid therapy with normal saline. Occasionally, an obstruction at the external urethral orifice can be dislodged by gentle massage. Sometimes, when a portion of the urethra is dilated with fluid under pressure and then suddenly released, urethral calculi can be flushed out. The urolith nearly always can be flushed back into the bladder by using the largest catheter that can be easily passed to the calculus, occluding the distal end of the urethral lumen around the catheter, and infusing a sterile mixture of equal parts of isotonic saline solution and an aqueous lubricant. If the urethrolith cannot be flushed back into the bladder, a urethrotomy should be performed to remove the obstructing stone(s). Depending on the clinical circumstances, the urethrotomy site may be sutured or a permanent urethrostomy created. Calculi flushed back into the bladder should be removed by cystotomy to prevent recurrence, although in some cases they can be dissolved. The stone should be sent for quantitative analysis, with the animal managed medically to prevent stone recurrence based on the results.
The most common canine uroliths are magnesium ammonium phosphate, calcium oxalate, or urate; less common uroliths include cystine, silica, calcium phosphate, and xanthine. While general management includes surgical removal and medical management, the appropriate treatment protocol depends on the location of the urolith and its chemical composition, as well as on patient-specific factors. Nephrolithiasis is generally not associated with an increase in the rate of progression of kidney injury; thus, it is recommended that animals with nephrolithiasis be managed without surgery in most cases.
The most common urinary stones in dogs are composed of struvite. The mineral composition is mostly struvite (MgNH4PO4 · 6H2O), but frequently, small amounts of carbonate-apatite and ammonium urate are present. In most cases, struvite uroliths form in association with urinary tract infections with urease-producing Staphylococcus or Proteus spp. Although they are frequent in cats, sterile struvite uroliths rarely form in dogs. They have been detected in a family of English Cocker Spaniels, suggesting a genetic predisposition.
Medical management involves dissolution and prevention of stone formation. In both instances, the aim of treatment is to reduce the concentrations of NH4+, Mg2+, and PO4-3 in urine. For dissolution, urine should be extremely undersaturated for struvite; for prevention, the degree of struvite saturation should be sufficiently low to make crystallization unlikely. The choice between surgery, lithotripsy, and medical treatment may not be easy. Owner compliance, the animal’s acceptance of the diet, availability of lithotripsy, practice philosophy, and knowledge of the indications and contraindications are necessary to make a decision. If stone dissolution is prolonged or fails, it may be more costly than surgical treatment. Surgical removal of uroliths is often incomplete, with small, hidden uroliths often inadvertently left in the urinary tract serving as a nidus for recurrence.
Before beginning stone dissolution by medical therapy, a physical examination, CBC, serum chemistry profile, urinalysis, urine culture and sensitivity, abdominal radiographs to document stone size, and blood pressure measurement (if possible) should be performed. Contraindications to stone dissolution include heart failure, edema, ascites, pleural effusion, hypertension, hepatic failure, renal failure, and hypoalbuminemia. However, chronic kidney disease is not always a contraindication for dissolution of struvite nephroliths.
While the use of urinary acidification to reduce urine pH to <6 and other individualized dietary maneuvers may prove effective, a few commercially available diets that are generally nutritionally balanced promote struvite stone dissolution. Dogs fed these rations generally have reduced intake of protein, phosphate, and magnesium and a high intake of sodium. This results in osmotic diuresis, reduced daily urea output, and enhanced urine volume. The low urinary urea concentration is one of the most important features of such diets and also reduces ammonia production by the action of urease-producing bacteria. No other food, including treats, should be fed, and adequate fresh water should be available at all times.
Urease-producing urinary tract infections must be treated. The choice of antibacterial should be based on sensitivity testing when possible. Most Staphylococcus and Proteus infections are sensitive to levels of amoxicillin or ampicillin achieved in the urine of healthy dogs. A urease inhibitor can be given but is not usually necessary. Concurrent treatment with a urease inhibitor such as acetohydroxamic acid enhances the rate of struvite stone dissolution, particularly when antibiotic resistance precludes effective antibacterial sterilization of the urine. A reasonably safe dose of acetohydroxamic acid appears to be 12.5 mg/kg, PO, bid. A reversible, mild hemolytic anemia has been seen in dogs given higher dosages.
After ~4 wk of treatment, a physical examination, serum chemistry profile, urinalysis, and abdominal radiographs or ultrasonography should be repeated. The stone dissolution protocol should be discontinued if severe adverse effects develop, although a mild degree of hypoalbuminemia is to be expected and can be tolerated. With good compliance, the following results can be anticipated: urine pH <6.5, urine specific gravity <1.025, serum urea <10 mg/dL. The radiographic stone size should be compared with the size on previous radiographs. Routine testing should be repeated every 4 wk until 4 wk after the stone is no longer visible radiographically; this generally takes 8–12 wk but may take as long as 20 wk. Stones that fail to reduce in size after 8 wk of treatment are probably not composed of struvite and should be treated another way, although failure could also result from poor treatment compliance. Renal stones tend to dissolve more slowly than bladder stones.
The recurrence rate after surgical treatment of struvite uroliths has been reported to be ~20%–25%, with most recurrences within 1 yr. When surgery is performed to remove multiple small struvite calculi, removing all stone material is often difficult. In such cases, a 4-wk dissolution protocol starting at the time of suture removal aids in preventing recurrence due to residual crystalline material. Once the urinary tract is free of stones, prevention strategies are much more likely to be successful.
The key to prevention of recurrence in animals with a struvite stone associated with infection is to achieve and maintain sterile urine. Routine testing of urine pH by the owner is important. If fresh urine is alkaline, a urinalysis and culture should be done, with the dog treated appropriately if an infection is present.
Once stone dissolution is completed, a prevention program can be considered. The aim is to prevent urinary tract infections with urease-producing microbes. The concentration of major struvite solutes in urine should also be reduced. A commercially available diet may be fed to lower urinary phosphate and magnesium and to maintain an acidic urine. Urease-producing infections should be eliminated, after which owners should regularly check the pH of the first voided urine in the morning after an overnight fast; in most dogs on a normal diet, the urine will be acidic. Checking urine pH weekly is sufficient.
Calcium oxalate uroliths have been increasing in frequency in dogs. Although they may develop in any breed, Miniature Schnauzers, Lhasa Apsos, Yorkshire Terriers, Bichon Frises, Shih Tzus, and Miniature Poodles may be predisposed. Most affected dogs are 2–10 yr old. Hypercalciuria leading to calcium oxalate stone formation can result from increased renal clearance of calcium due to excessive intestinal absorption of calcium (absorptive hypercalciuria), impaired renal conservation of calcium (renal leak hypercalciuria), or excessive skeletal mobilization of calcium (resorptive hypercalciuria).
Absorptive hypercalciuria is characterized by increased urine calcium excretion, normal serum calcium concentration, and normal or low serum parathormone concentration. Because absorptive hypercalciuria depends on dietary calcium, the amount of calcium excreted in the urine during fasting is normal or significantly reduced when compared with nonfasting levels. Renal leak hypercalciuria has been recognized in dogs less frequently than absorptive hypercalciuria. In dogs, renal leak hypercalciuria is characterized by normal serum calcium concentration, increased urine calcium excretion, and increased serum parathormone concentration. During fasting, these dogs do not show a decline in urinary calcium loss. The underlying cause of renal leak hypercalciuria in dogs is not known. Resorptive hypercalciuria is characterized by excessive filtration and excretion of calcium in urine as a result of hypercalcemia. Hypercalcemic disorders have been associated only infrequently with calcium oxalate uroliths in dogs.
Routine laboratory determinations should include serum calcium, phosphate, total CO2, and chloride to eliminate the possibility of hyperparathyroidism and renal tubular acidosis. Dissolution of calcium oxalate stones by medical means has not currently been established. Treatment requires surgical removal or lithotripsy followed by preventive strategies.
Recurrence is a major problem with calcium oxalate uroliths. An “ideal” diet is considered to be low oxalate, low protein, and low sodium and would maintain urine pH at 6.5–7.5 and urine specific gravity <1.020. A few commercially available canned foods achieve these goals and may minimize the risk of recurrence. Potassium citrate may be added as needed to assure the urine pH is within the desired range; water may be used to provide appropriate reduction in urine concentration. If these urine conditions are achieved and calcium oxalate crystals are still seen in warm, fresh urine, then vitamin B6 and/or thiazide diuretics can be considered (although of unproven efficacy). Effectiveness of therapy should be reevaluated at 1- to 4-mo intervals by urinalysis. Chlorothiazide diuretics may also be of value.
Ammonium urate stones are most common in Dalmatians and in dogs with congenital portosystemic vascular shunts. The formation of ammonium urate calculi depends on the urine concentrations of urate and ammonium and on other poorly understood factors. Dalmatians do not convert most of their metabolic urate to allantoin and thus excrete the bulk of nucleic acid metabolites as relatively insoluble urate. The biologic mechanism responsible for decreased hepatic conversion of urate to allantoin lies not in reduced uricase activity but in reduced hepatic transport of urate; the rate of urate hepatic transport is approximately three times faster in breeds other than Dalmatians. The net result is that only 30%–40% of urate is converted to allantoin in Dalmatians compared with ~90% in other breeds.
Dalmatians fed a diet high in animal protein excrete a net acid load in the urine, and urinary ammonium output is subsequently increased. The combined high concentration of ammonium and urate in urine increases the risk of formation of ammonium urate stones. The excretion of acidic metabolites of an animal protein diet is believed to be important in this process, because urinary ammonium excretion is enhanced and ammonium urate is insoluble. Urate output has been reported to be the same in Dalmatians that form stones and in those that do not, although in some studies the methods used to determine urine uric acid concentrations were unreliable. In dogs with a portosystemic vascular anastomosis, increased urinary ammonium output may partially be due to the increased filtered load of ammonia, because plasma levels of ammonia tend to be increased.
Urine alkalinization minimizes renal ammonia production; the goal is to achieve a urine pH >7. If required, urine alkalinization can be achieved by administering NaHCO3, 1 g (¼ tsp)/5 kg, PO, tid, with food. Potassium citrate, administered to effect (25–50 mg/kg/day) is an alternative, more palatable alkalinizing agent.
Urinary urate output should be reduced. This can be accomplished by feeding a low-purine, low-protein commercial diet. In addition, the xanthine oxidase inhibitor allopurinol (15 mg/kg, PO, bid) may be administered to ensure the nucleic acid metabolite load is excreted as a combination of xanthine, hypoxanthine, uric acid, and allantoin, rather than almost entirely as urate. However, the effectiveness of allopurinol in reducing urinary urate output is variable, and urinary urate levels should be measured (although this may be difficult). Allopurinol must be used cautiously in dogs with hepatic disease or primary renal failure, because it is metabolized to its active form in the liver and is excreted via the kidneys. It is important that diets high in purines not be fed to dogs receiving allopurinol because xanthine uroliths may result.
Urine volume should be increased to reduce the concentration of all dissolved solutes in urine. This can be achieved by feeding canned diets restricted in protein. By reducing formation of urea, renal medullary urea concentration declines, interfering with the countercurrent system of urine concentration. Adding salt, 1 g (¼ tsp)/5 kg, daily to the diet, or mixing water with the food are additional methods. Salt should not be given to animals with hypertension but otherwise poses little risk in normotensive dogs without chronic kidney disease, proteinuria, or hypoalbuminemia.
Prevention strategies aim to reduce the concentration of ammonium and urate in urine to levels unlikely to induce flocculation.
A low-protein, low-purine diet should be fed to reduce urinary urate output. Alkalinization should be used as needed to ensure alkalinuria. Treatment with allopurinol (10 mg/kg/day, PO) can be considered. Ideally, allopurinol is not needed as a supplement to dietary management; however, if urate crystals persist, a low-maintenance dose of allopurinol is appropriate.
These dissolution and prevention strategies were developed for use in Dalmatians in which hepatic conversion of urate to allantoin is reduced but the liver is otherwise normal. They may not be safe for use in dogs with portosystemic vascular shunts. Such dogs tend to develop hypoalbuminemia, edema, and ascites when fed a low-protein diet. The safety of allopurinol in these dogs has not been established. In addition, alkalinization can predispose to hepatic encephalopathy because of increased GI absorption of dietary protein metabolites.
Stones composed almost entirely of cystine form in dogs that have a renal tubular amino acid reabsorption defect known as cystinuria. Healthy dogs demonstrate 97% fractional reabsorption of cystine, whereas affected dogs excrete a much greater proportion of the filtered cystine load and may even exhibit net cystine secretion. Cystine is a relatively insoluble amino acid; therefore, in high concentration it may precipitate and form stones. Despite excessive urinary loss of cystine in cystinuric dogs, plasma cystine levels remain the same as in healthy dogs; in fact, the only morbidity or mortality associated with the inherited defect of cystine reabsorption is urolith formation. Identification of cystine crystals by urinalysis indicates the dog is at risk of forming cystine uroliths. For poorly understood reasons, not all cystinuric dogs develop uroliths. However, the absence of uroliths does not preclude their future development, and preventive measures are indicated.
Cystinuria is thought to be inherited as a sex-linked trait. However, in Newfoundlands it is transmitted as a simple autosomal recessive trait. The defect has also been reported in Dachshunds, Basset Hounds, English Bulldogs, Chihuahuas, Yorkshire Terriers, Irish Terriers, and mixed-breed dogs. Cystinuria has been recognized almost exclusively in male dogs, except in Newfoundlands. A urine cystine concentration of >75 mg/g creatinine in nonfasted dogs is predictive of susceptibility to cystine urolithiasis.
Cystine solubility depends on urine pH, with solubility increasing rapidly when urinary pH is >7.5. Dogs fed meat-based diets tend to excrete acidic urine, which leads to urine cystine supersaturation.
Cystinuria is a lifelong defect of tubular reabsorption and cannot be cured. Cystine stones tend to recur within 1 yr without management to prevent recurrence, and they often recur despite attempts at prevention.
Urinary cystine output should be reduced. Protein-restricted alkalinizing diets have been associated with reducing the size of cystine urocystoliths. Urinary cystine concentration can also be reduced by administering N-(2-mercaptoproprionyl)-glycine (2-MPG, tiopronin) or penicillamine. 2-MPG should be given at 15–20 mg/kg, PO, bid, for dissolution, and at 10–15 mg/kg, PO, bid, for prevention. Penicillamine (15 mg/kg, PO, bid) can be substituted for 2-MPG; unfortunately, ~40% of dogs treated with penicillamine exhibit anorexia and vomiting. The vomiting may be partially resolved by giving the medication with meals; however, a severe reduction in dosage or complete withdrawal is often necessary.
The urine should be alkalinized to a pH >7.5. Sodium bicarbonate added to the diet at 1 g (¼ tsp)/5 kg, tid, readily accomplishes this, but because sodium supplementation may enhance cystinuria, potassium citrate (20–75 mg/kg, PO, bid) is preferred.
Urine volume can be increased by mixing water with the food. Salt should not be added to the diet, because increased sodium excretion may cause increased cystine excretion. If urine volume is adequate and the urine pH is maintained above 7.5, most cystinuric dogs will pass urine that is only slightly supersaturated or undersaturated for cystine. Under such conditions, only relatively small doses of 2-MPG or penicillamine may be necessary to achieve 24-hr undersaturation.
Early reports indicated a predominance of silica stones in German Shepherds, but many breeds have now been implicated. Urethral obstruction in males is the most common presenting problem, but signs similar to those associated with other types of uroliths also may be noted. The mean age at occurrence is ~6 yr. The stones are usually multiple and develop in the bladder and urethra. Silica uroliths are radiopaque. They frequently, but not always, have a characteristic “jackstone” appearance. Identification requires spectrographic analysis and cannot be made with kits for qualitative stone analysis.
The role of diet in spontaneously occurring silica urolithiasis has not been determined, although plants are often an abundant source of silica. If the diet of an affected dog is known to be high in silica, or if silica urolithiasis has been recurrent, a dietary change should be recommended. Only general management principles can be suggested for silicate urolithiasis. Additional salt and/or water should be added to the diet to induce diuresis and to lower the urine solute concentration. When present, urinary tract infections should be eliminated. Diets high in plant proteins should be avoided.
(Feline urologic syndrome)
Hematuria, pollakiuria, and stranguria are the characteristic clinical signs of feline lower urinary tract disease (FLUTD) in cats. Although the specific underlying cause of this common syndrome is often not identified, associated conditions include urinary tract infection, neoplasia, trauma, urethral plugs, urolithiasis, and sterile cystitis (feline interstitial cystitis).
Feline urolithiasis is a common disease seen with equal frequency in both sexes. Until recently, it was thought that most uroliths in cats were small and resembled sand or were gelatinous plugs that differed from typical uroliths in that they contained a greater amount of organic matrix, giving them a toothpaste-like consistency. Matrix-crystalline plugs are most commonly found within the urethra near the urethral orifice and are primarily responsible for urethral obstruction. Recently, prevalence of urolithiasis with grossly observable stones composed primarily of calcium oxalate has increased in cats. The most common feline uroliths are calcium oxalate, magnesium ammonium phosphate, and urate.
Urolithiasis is usually suspected based on clinical signs of hematuria, dysuria, or urethral obstruction. Urinalysis, urine culture, radiography, and ultrasonography may be required to differentiate uroliths from urinary tract infection or neoplasia. Radiography, cystoscopy, or ultrasonography are critically important to detect uroliths, because only ~10% of feline urocystoliths can be detected by abdominal palpation. Uroliths with a diameter >3 mm are usually radiodense; however, because smaller uroliths are common, double-contrast radiography may be required for detection. Radiographic evidence of uroliths is seen in ~20% of cats with hematuria or dysuria.
The usual clinical approach to grossly observable urocystoliths is surgical removal or lithotripsy where available, followed by dietary therapy instituted as a preventive measure. For sterile struvite uroliths, medical dissolution is the preferred treatment. Nephrolithiasis is not associated with an increase in the rate of progression of feline kidney injury, and cats with nephrolithiasis are generally managed without surgery.
Calcium oxalate uroliths are the most common feline uroliths and the most common nephrolith, although their underlying cause is unknown. Common management schemes that involve feeding urine-acidifying diets with reduced magnesium have reduced the incidence of feline struvite urolithiasis. Magnesium has been reported to be an inhibitor of calcium oxalate formation in rats and people; thus, the reduced magnesium concentration in feline urine may partially explain the increase in calcium oxalate stones in cats.
Medical protocols that promote calcium oxalate dissolution are not known; therefore, surgery and lithotripsy are the primary means for removal (small bladder stones may be eliminated by voiding urohydropulsion). However, some calcium oxalate uroliths, especially those in the kidneys, may not cause clinical signs for months to years. Because of the unavoidable destruction of nephrons during nephrotomy, this procedure is not recommended unless it can be established that the stones are a cause of clinically significant disease. Recurrence remains problematic. A variety of diets has been formulated to restrict the formation of calcium oxalate uroliths and should be considered appropriate for maintenance in cats with nephroliths and after the removal of urocystoliths. Diets that reduce the likelihood of formation of both struvite and calcium oxalate stones are commercially available. Eliminating any associated urinary tract infections, avoiding mineral and vitamin C and D supplementation, and encouraging water consumption are critical.
Three distinct types of struvite uroliths are recognized in cats: amorphous urethral plugs with a large quantity of matrix, sterile struvite uroliths (which form perhaps as a result of certain dietary ingredients), and struvite uroliths that form as a sequela of urinary tract infection with urease-producing bacteria. Struvite uroliths induced by infection are less common than sterile struvite uroliths. An additional type of struvite urolith in cats consists of a sterile struvite nidus that predisposes to urinary tract infection with urease-producing bacteria and subsequent formation of infected struvite laminations around the sterile nidus.
Treatment of sterile struvite urolithiasis focuses on reducing the urine pH to ≤6 and on reducing the urine magnesium concentration by feeding magnesium-restricted diets. Reducing urine pH and magnesium concentration is best accomplished by feeding a commercially available prescription diet formulated for this purpose. Some diets are formulated to reduce the formation of both struvite and calcium oxalate stones. Generally, neither sodium chloride nor urine acidifiers should be given concurrently with these diets, because they are already supplemented with sodium chloride and formulated to produce aciduria. In addition, these diets should not be fed to cats that are acidemic, have azotemia of any cause, or have cardiac dysfunction or hypertension. Urolith size should be monitored every 4 wk by radiographs or ultrasonography, and crystalluria by urinalysis. Struvite crystals should not form if therapy has been effective in producing urine that is undersaturated with magnesium, ammonium, and phosphate. Because small uroliths may not be detected radiographically, the calculolytic diet should be continued for ≥4 wk after radiographic documentation of urolith dissolution. If treatment does not induce complete dissolution of uroliths, it is likely that either the wrong mineral component was identified, the nucleus of the urolith is composed of a different mineral than the outer portion of the urolith, or the owner is not complying with therapeutic recommendations.
Ammonium urate, uric acid, calcium phosphate, and cystine uroliths are less common in cats, but ammonium urate and uric acid account for ~6% of feline uroliths. Although a renal tubular reabsorptive defect and portovascular anomalies have been incriminated as causes in a few cases, the cause of most urate uroliths in cats has not been established. Nonetheless, formation of highly acidic and concentrated urine associated with consumption of diets high in purine precursors (especially liver) appears to be a risk factor.
Medical protocols that consistently promote dissolution of ammonium urate uroliths in cats have not been developed, and surgery remains the most common method of removal. For small stones, voiding urohydropulsion may be effective. Prevention should include feeding a diet low in purine precursors and promoting formation of less acidic urine that is not highly concentrated. Although allopurinol may reduce the formation of urate in cats, studies of the efficacy and potential toxicity of allopurinol in cats are required before meaningful guidelines can be established.
Feline interstitial cystitis is generally taken to be synonymous with sterile cystitis of unknown cause. The underlying cause of this disorder is unknown, although anxiety and altered neurohormonal factors have been implicated.
Diagnosis is by exclusion of other causes of lower urinary tract disease in cats, such as obstruction by urethral plugs, bacterial urinary tract infection, neoplasia or other mass lesions, and urolithiasis. Diagnostic tests to exclude these conditions may include radiographs, ultrasonography, urinalysis, urine culture, and cystoscopy.
Because the cause of feline interstitial cystitis is unknown, the goal of treatment is to reduce the severity and frequency of episodes of cystitis. Therapeutic considerations include reduction of stress through environmental changes, dietary adjustments (eg, use of canned preparations), pheromones applied topically in the environment, and analgesics (eg, butorphanol, 0.2–0.4 mg/kg, PO, bid-tid). Other medications (eg, amitriptyline, 5–12.5 mg/cat, PO, once or twice daily; clomipramine, 0.5 mg/kg/day, PO; fluoxetine, 1 mg/kg/day, PO) have yielded mixed results.