Pathophysiology<\/h2>\nStruvite Uroliths<\/h3>\n
In cats, approximately 45% of uroliths consist entirely or predominantly of struvite, and most feline struvite uroliths form in sterile urine (Figure 1<\/strong>).1<\/sup> The pathophysiology of struvite urolith formation in sterile urine is poorly understood; however, dietary and metabolic factors that result in alkaline urine and increased concentrations of magnesium, ammonium, and phosphate in urine have been implicated.<\/p>\n Dietary Factors.<\/strong> Diets high in magnesium, phosphorus, calcium, sodium, chloride, and fiber, with moderate protein content have been associated with increased risk.2<\/sup> A greater ability to concentrate urine (compared with dogs, in which struvite uroliths are commonly associated with infection) and, therefore, greater urine supersaturation, may be partially responsible for urolith formation in cats without urinary tract infections (UTIs).<\/p>\n Metabolic Factors.<\/strong> In addition, formation of sterile struvite uroliths may be twice as likely if urine pH is consistently elevated (6.5\u20136.9 versus 6\u20136.2).2<\/sup> Alkaline urine pH is commonly affected by diet but may also be associated with drug therapy and renal tubular disorders. In 1981, more than 80% of the feline uroliths analyzed at the Minnesota Urolith Center were struvite.3<\/sup> A major factor contributing to the decline in feline struvite uroliths over the last 35 years is the widespread use of magnesium-restricted, acidifying diets.<\/p>\n Infection.<\/strong> Struvite uroliths in cats may be associated with UTI, especially when caused by bacteria that produce urease, such as Staphylococcus<\/em> and Proteus<\/em> species. In such cases, urease increases the ammonium concentration in urine, resulting in an increase in urine pH and a change in the ionization state of phosphorus. Interestingly, struvite uroliths associated with UTI tend to be more radiodense than struvite uroliths that form in sterile urine.4<\/sup><\/p>\n FIGURE 1. Lateral radiograph of a 6-year-old spayed female domestic shorthair cat with multiple struvite cystoliths (A); 80% struvite, 20% ammonium acid urate cystoliths were removed from this cat (B). (Scale, 1 division = 1 mm)<\/p><\/div>\n Factors involved in the pathogenesis of calcium oxalate urolithiasis (Figure 2<\/strong>) in cats are not completely understood but involve urine supersaturation with calcium and oxalate:<\/p>\n Dietary and Metabolic Factors.<\/strong> As with struvite uroliths, diet can also influence the development of calcium oxalate uroliths. Cats fed low-sodium or low-potassium diets or diets formulated to maximize urine acidity are at increased risk.2,6<\/sup><\/p>\n In 1981, less than 10% of the feline uroliths analyzed at the Minnesota Urolith Center were calcium oxalate; in 2013, that percentage had increased to 41%.3<\/sup> Use of acidifying diets is thought to have played a role in this increase: diets that produce a urine pH between 6 and 6.2 are 3 times more likely to produce calcium oxalate uroliths when compared with acidifying diets designed to produce a urine pH between 6.5 and 6.9.2<\/sup><\/p>\n In addition, metabolic acidosis increases calcium mobilization from bone and contributes to hypercalciuria as well as decreased urinary citrate excretion.<\/p>\n FIGURE 2. Lateral radiograph of a 9-year-old castrated male domestic longhair cat with calcium oxalate cystoliths (A); 100% calcium oxalate monohydrate cystoliths were removed from this cat (B). (Scale, 1 division = 1 mm).<\/p><\/div>\n Recurrence of calcium oxalate uroliths in cats is a potential problem. In a study of more than 2000 cats with calcium oxalate uroliths, 7% had a first recurrence, 0.6% had a second recurrence, and 0.1% had a third recurrence.12<\/sup> These results underscore the need for medical protocols aimed at decreasing recurrence of calcium oxalate uroliths after urolith removal.<\/p>\n Clinical signs of urolithiasis in cats depend on urolith number, location, and physical characteristics. Solitary, smooth uroliths in the bladder or renal pelvis may be less irritating than multiple uroliths or uroliths with irregular or sharp borders. Urolithiasis complicated by bacterial UTI is more likely to cause tissue inflammation than sterile urolithiasis.<\/p>\n Nephroliths are often asymptomatic but can be associated with microscopic or gross hematuria. All nephroliths have potential to damage renal tissue and cause chronic inflammation; this chronic inflammation may decrease normal host defense mechanisms and increase the risk for ascending bacterial pyelonephritis in cats with lower UTIs.<\/p>\n Larger nephroliths can cause hydronephrosis associated with pelvic and\/or ureteral obstruction. Smaller nephroliths may pass through the ureter asymptomatically; however, hydroureter and hydronephrosis may be secondary to urolith-induced ureteral obstruction or stricture.<\/p>\n Ureteroliths may be asymptomatic or associated with varying degrees of abdominal pain and decreased appetite. In cats with pre-existing CKD, partial or complete ureteral obstruction will often result in an \u201cacute-on-chronic\u201d decompensation of renal function that may include hyperkalemia and\/or acidemia. Ureteral obstruction in a cat with previously normal renal function may not be associated with any clinicopathologic abnormalities, especially if it is unilateral, but renal asymmetry may be palpated due to hydronephrosis.<\/p>\n Cystoliths may be asymptomatic or, instead, irritate the uroepithelium, resulting in hematuria, pollakiuria, and dysuria\/stranguria. Struvite cystoliths can result from urease-producing bacterial UTI; however, any urocystolith can irritate the uroepithelium, compromise host defense mechanisms, and predispose the patient to a complicated bacterial UTI.<\/p>\n Urethral uroliths are common causes of partial or complete urethral obstruction in males, leading to an altered or absent urine stream, hematuria, or dysuria\/stranguria. In cases of complete urethral obstruction, postrenal azotemia and uremia develop within 24 to 36 hours.<\/p>\n \u00a0Types of Uroliths<\/strong><\/p>\n Nephrolith:<\/strong> Calculus formed or retained in the kidney<\/p>\n Ureterolith:<\/strong> Calculus located in the ureter<\/p>\n Cystolith:<\/strong> Calculus formed or retained in the bladder; also called vesical calculus<\/p>\n Urethral urolith:<\/strong> Calculus located in the urethra<\/p><\/blockquote>\n The number, mineral composition, size, and location in the urinary tract affect the radiographic and ultrasonographic appearance of uroliths.<\/p>\n Indications for imaging besides radiography include:<\/p>\n FIGURE 3. Ultrasound image of dilated ureter with ureterolith.<\/p><\/div>\n FIGURE 4. Ultrasound image of dilated renal pelvis (pyelectasia) associated with ureteral obstruction.<\/p><\/div>\n FIGURE 5. Positive contrast antegrade pyelogram demonstrating pyelectasia and ureteral obstruction due to a ureterolith.<\/p><\/div>\n Transurethral cystoscopy may be performed in both male (flexible scope) and female (rigid scope) cats for the diagnosis of cystoliths; however, general anesthesia is required. In female cats, holmium:YAG laser lithotripsy associated with cystoscopy may be used to noninvasively \u201cbreak up\u201d cystoliths and remove them from the bladder without surgery. Cystoscopy may also be used to obtain biopsy tissue from the lower urinary tract.<\/p>\n Urine pH, crystalluria, and presence of urease-producing bacteria may aid in the presumptive identification of urolith type. Serum ionized calcium concentrations should be assessed in cases of suspected calcium oxalate uroliths to rule out hypercalcemia.<\/p>\n Uroliths may be caused by a UTI (struvite) or may compromise normal host defense mechanisms and predispose cats (especially female cats) to UTI. Therefore, a urine culture should be routinely performed.<\/p>\n Definitive diagnosis requires quantitative mineral analysis of uroliths that have been voided or recovered from the urinary tract.<\/p>\n General principles for treatment of urethral calculi include relief of urethral obstruction and bladder decompression, if necessary, which can usually be accomplished by:<\/p>\n Fluid therapy should be initiated to restore water and electrolyte balance, if postrenal azotemia exists.<\/p>\n Surgical intervention for calcium oxalate nephroliths (beyond dietary treatment\u2014see Calcium Oxalate Uroliths<\/strong>\u2014to help slow urolith growth) is usually not recommended. Similarly, surgical intervention of ureteral uroliths is usually not recommended. In both cases, the complication rate associated with surgery (eg, compromised renal function and ureteral stricture) is high.<\/p>\n Cats with obstructive ureterolithiasis are best managed with ureteral stents or subcutaneous ureteral bypass (SUB). Intracorporeal laser lithotripsy via cystoscopy may be used to treat cystoliths in female cats.<\/p>\n Hyperkalemia is a potentially life-threatening electrolyte disturbance that may occur in cats with postrenal azotemia caused by urethral obstruction or rupture of the urinary bladder or urethra. In cats suspected of having urethral obstruction, findings that suggest hyperkalemia include:<\/p>\n These findings indicate the need for emergency treatment to decrease the serum potassium concentration prior<\/em> to sedation\/anesthesia for urethral catheterization.<\/p>\n Medical dissolution of feline struvite uroliths is effective; however, the decision to proceed surgically as opposed to medically involves several considerations (Table 1<\/strong>).<\/p>\n Diet.<\/strong> Struvite dissolution diets (Table 2<\/strong>) are magnesium-reduced, acidifying diets. Due to their high sodium content and acidifying nature, these diets should not<\/em> be fed to immature cats; reproducing queens; or cats with CKD, hypertension, congestive heart failure, postrenal azotemia\/uremia, or hypokalemia. Additional supplementation of sodium chloride and\/or urinary acidifiers is not<\/em> recommended with use of dissolution diets.<\/p>\n It is ideal to transition from the normal diet to the dissolution diet over a period of at least 1 week. Reradiograph cats on dissolution diets every 2 to 4 weeks, and feed the diet for a minimum of 30 days after the uroliths are no longer visible radiographically. The rate at which uroliths dissolve is proportional to the surface area of the urolith exposed to the undersaturated urine. Small, sterile struvite uroliths may dissolve in as little as 1 to 2 weeks.14<\/sup><\/p>\n Struvite dissolution diets do not dissolve nonstruvite uroliths and are less effective if a persistent UTI is present or the cat is fed anything in addition to the dissolution diet.14,15<\/sup><\/p>\n Antibiotics.<\/strong> In addition to decreasing the concentration of crystalloids in urine, elimination of any bacterial UTI is essential in medical treatment of struvite urolithiasis. If infection is present at start of treatment, continue antibiotics throughout the course of medical dissolution because viable bacteria may be released from uroliths as they dissolve. Select antibiotics based on urine culture and sensitivity findings. Infection-induced struvite uroliths usually dissolve in 2 to 3 months.15<\/sup><\/p>\n Medical dissolution diets for oxalate urolithiasis are not yet available. Small urocystoliths may be removed by catheter retrieval or voiding hydropropulsion in female cats; however, surgery is the usual means for removal of large calcium oxalate cystouroliths.<\/p>\n Some calcium oxalate uroliths, especially nephroliths, may remain clinically quiescent for months to years. Cats with CKD, and with suspected calcium oxalate nephroliths, had no increased risk for kidney disease progression, uremic crises, or death compared with cats with similar stage CKD without nephroliths.16<\/sup> Manage patients with nephroliths with medical protocols designed to prevent or slow calcium oxalate urolith growth (see Prevention<\/strong>), and monitor location and size of the nephroliths several times a year with radiography or ultrasonography.<\/p>\n Acute decompensation of a patient with CKD and known or suspected nephroliths should prompt swift evaluation to rule out an obstructive uropathy.<\/p>\n Measures to prevent struvite urolith recurrence include preventing and controlling UTIs in cases of infection-induced struvite uroliths, maintaining acidic urine, and decreasing dietary intake of magnesium. Numerous struvite prevention maintenance diets are available commercially (Table 3<\/strong>).<\/p>\n![\"FIGURE](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/09\/T1509F01_Fig01_REV.jpg\")
<\/a>Calcium Oxalate Uroliths<\/h3>\n
\n
<\/a>Risk Factors<\/h2>\n
Struvite Uroliths<\/h3>\n
\n
Calcium Oxalate Uroliths<\/h3>\n
\n
Clinical Signs<\/h2>\n
Nephroliths<\/h3>\n
Ureteroliths<\/h3>\n
Cystoliths<\/h3>\n
Urethral Uroliths<\/h3>\n
Diagnosis<\/h2>\n
Imaging<\/h3>\n
\n
\n
<\/a><\/a><\/a>Cystoscopy<\/h3>\n
Laboratory Findings<\/h3>\n
Definitive Diagnosis<\/h3>\n
Treatment<\/h2>\n
\n
Surgical Therapy<\/h3>\n
Emergent Therapy<\/h3>\n
\n
Struvite Uroliths<\/h3>\n
<\/a><\/p>\n<\/a><\/p>\nCalcium Oxalate Uroliths<\/h3>\n
Follow-up and Monitoring<\/h2>\n
\n
Prevention<\/h2>\n
Struvite Uroliths<\/h3>\n