2. In general, pharmacological agents should be added in stepwise fashion, with the goal of reducing the urine concentration
of calculogenic substances. Medications that have the potential to induce a sustained alteration in body composition of metabolites,
in addition to urine concentration of metabolites, should be reserved for patients with active or frequently recurrent uroliths.
Caution must be used so that the side effects of treatment are not more detrimental than the effects of the uroliths.
3. Oral administration of potassium citrate is of proven value in minimizing recurrence of CaOx uroliths in humans. The benefit
is related to increased urinary excretion of citric acid and subsequent formation of calcium citrate. Calcium citrate is much
more soluble in urine than calcium oxalate. However, oral administration of calcium citrate to dogs is not associated with
increased urinary excretion of citric acid.
The effect of potassium citrate on urine citric acid concentrations in cats with CaOx uroliths has not been well documented.
Even though oral administration of potassium citrate may not be associated with a sustained increase in urine citrate excretion,
it may be useful in patients with acidosis-induced hypercalciuria because of its alkalinizing effects. The oral dosage commonly
used is 40 to 75 mg/kg every 12 hours. The dose may be adjusted by evaluation of serum total carbon dioxide concentrations,
blood bicarbonate concentrations and/or urine pH. Appropriate precautions should be taken to prevent iatrogenic hyperkalemia.
4. Vitamin B6 has been recommended for management of calcium oxalate uroliths because it reversed hyperoxaluria in kittens
fed a vitamin B6 deficient diet. The efficacy of supplemental vitamin B6 in reducing urinary oxalate excretion in cats with
CaOx uroliths has not been determined. However, empirical use of this inexpensive nutrient at an oral dose of 2 to 4 mg/kg
is apparently safe.
5. Thiazide diuretics decrease urinary excretion of calcium in humans and dogs with CaOx uroliths. However, the safety and
efficacy of thiazides has not been documented in cats. Because they have the potential to induce dehydration and electrolyte
imbalances (hypokalemia and hypercalcemia), we cannot recommend their routine use.
6. Glucocorticoids promote urinary excretion of calcium and therefore have been empirically recommended to treat cats with
CaOx uroliths and idiopathic hypercalcemia. However, the long-term safety and efficacy of glucocorticoids in this situation
have not been documented in controlled clinical trials. Therefore, they should be used with appropriate caution.
7. We have had some success in correcting idiopathic hypercalcemia associated with CaOx uroliths by feeding a high fiber diet
(Prescription Diet Feline w/d-Hill's) and supplemental oral potassium citrate. As with glucocorticoid therapy, further clinical
studies are needed to evaluate the long-term safety and efficacy of this regimen.
Monitoring responseMedical prevention protocols should be consistently monitored by appropriate indices of therapeutic response. These typically
include timely urinalyses, serum chemistry profiles, and radiography or ultrasonography. Therapy should be adjusted to meet
each individual patient's needs. The degree to which risk factors have been eliminated or modified should be considered when
determining the frequency of re-evaluations (Table 2).
A large number of persistent risk factors warrants more frequent rechecks. If urocystoliths recur despite efforts to minimize
risk factors, early detection will facilitate their removal by voiding urohydropropulsion.