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An Urban Experience
in association with either hypercalcemia (eg, primary hyperparathyroidism, idiopathic hypercalcemia in cats) or normocalcemia.6 Selection of effective preventative treatment is challenging because (1) properly designed clinical trials evaluating urolith recurrence have not been published, (2) the exact mechanisms underlying calcium oxalate urolith formation are not completely understood, (3) associative factors identi ed in epidemiological studies have not been proven to result in disease, and (4) surrogate endpoints of therapeutic ef cacy such
as relative supersaturation are mathematical models
that may not correlate well with calcium oxalate urolith formation. The high recurrence rate of calcium oxalate uroliths warrants a comprehensive approach and regular monitoring. High-moisture (>75% water) foods or adding water to dry food should be recommended. Strive to achieve a urine speci c gravity ≤1.020 in dogs and <1.030 in cats Increasing dietary protein from 35% to 57% (dry matter) increased urine calcium concentration by 35% and decreased urine citrate concentration by 45% in cats.62 In dogs and cats with hypercalcemia, correcting or controlling hypercalcemia aids in preventing calcium oxalate urolith recurrence. Doing so is dif cult
in cats with idiopathic hypercalcemia and no single treatment has been shown to be effective, including glucocorticoids, bisphosphonate administration, or dietary modi cation using a high- ber diet with potassium citrate administration.22 Feeding high-sodium (>375 mg/100 kcal) dry foods should not be a recommended as a substitute for high-moisture foods. High-sodium foods increase urinary water excretion, but the effects appear to be short-lived (ie, 3– 6 months).23 Potassium citrate is an alkalinizing salt that when administered
PO and metabolized promotes the excretion of more bene cial alkaline urine. Alkaline urine enhances urinary citrate excretion, which is a chelator of calcium ions. Consider thiazide diuretics for frequently recurrent calcium oxalate uroliths as they enhance the renal tubular reabsorption of  ltered calcium. Some recommend the concomitant administration of potassium citrate because thiazide diuretics contribute to urine acidi cation. A
55% decrease in urinary calcium concentration was reported in urolith-forming dogs that were treated with hydrochlorothiazide at a dosage of 2 mg/kg q12h.24
A 65% decrease in urinary calcium oxalate relative supersaturation was reported in clinically normal cats receiving hydrochlorothiazide at a dosage of 1 mg/kg q12h.25 In order to minimize urate urolith recurrence, decrease urine concentration, promote alkaline urine, and limit purine intake. For dogs with the SLC2A9 mutation, urate urolith recurrence can be minimized by increasing  uid intake, promoting alkaline urine (pH ≥ 7), and limiting purine intake. In cats and dogs with porto- vascular anomalies, correcting of the vascular anomaly should also be considered, if appropriate. Data in cats are limited, but purine restriction and urine alkalization are recommended. High-moisture (>75% moisture)
foods or adding water to dry food is recommended. Strive to achieve a urine speci c gravity ≤1.020 in dogs and <1.030 in cats. Additional water consumption to achieve lower urine concentrations of uric acid provides more effective prevention. Urate solubility increases
with increasing urine pH.13 Decreasing dietary protein has been shown to decrease urinary saturation with ammonium urate in dogs. Selecting an effective food may be dif cult because properly controlled studies evaluating urolith recurrence are rare. Consider xanthine oxidase inhibitors for dogs homozygous for genetic hyperuricosuria that have failed therapeutic diet prevention. Use a dosage of 5–7 mg/kg q12–24 h to safely prevent urate uroliths. Administration of xanthine oxidase inhibitors should be avoided in dogs that are not receiving decreased purine diets to minimize the risk of xanthine urolith formation. Xanthine oxidase inhibitors have not been formally investigated in cats. In order
to minimize cystine urolith recurrence, decrease urine concentration, limit animal protein intake, limit sodium intake, increase urine Ph, and neuter. Newer classi cation systems for cystinuria have been published recently.26 High-moisture (>75% moisture) foods or adding water
to dry food is recommended. Strive to achieve a urine speci c gravity ≤1.020 in dogs and <1.030 in cats. Cystine solubility increases with increasing urine pH. In vitro studies that achieved a urine pH > 7.5 increased
the ef cacy of thiol drugs to solubilize cystine in the urine of cystinuric humans. Therefore, potassium citrate or other alkalinizing citrate salts should be administered
to dogs and cats with persistently acidic urine. The dosage should achieve a urine pH of approximately 7.5. Diets for the prevention of cystine uroliths should be
low in methionine and cystine precursors with adequate amounts of taurine and carnitine. Feeding high-protein diets, particularly those rich in methionine, a cystine precursor, should be avoided in cystinuric dogs. In some forms of cystinuria, neutering has been associated
with decreases in cystine concentration because of a suspected androgen-dependent effect, but this effect
is not universal. In recurrent cystine urolith formers, add
2 mercaptopropionylglycine to prevention strategies to further lower cystine concentration and increase cystine solubility. Dosages are 15 mg/kg PO q12h.

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