11. In contrast to dietary calcium, consumption of non-dietary calcium supplements between meals has minimal effect on the intestinal absorption of oxalic acid derived from the diet. As a result, non-dietary calcium supplements increase the risk for CaOx urolith formation.

12. Dietary phosphorus restriction is a risk factor for increased urinary calcium excretion because diets deficient in phosphorus stimulate renal activation of vitamin D. Vitamin D, in turn, promotes intestinal absorption and subsequent urinary excretion of calcium. Reduction of dietary phosphorus may also result in reduced formation of relatively insoluble calcium phosphate complexes in the intestinal lumen, thereby enhancing intestinal absorption and renal excretion of calcium. Therefore, to minimize recurrence of CaOx uroliths, dietary phosphorus should not be restricted.

13. Diets formulated to acidify urine promote calcium oxalate uroliths by inducing hypercalciuria. The association between persistent aciduria and increased urolith formation is not directly related to decreased solubility of CaOx crystals in acid urine. CaOx crystals can form in acid and alkaline urine. The association between aciduria, acidemia, and calcium oxalate urolithiasis may be explained at least in part, by the fact that acidemia promotes mobilization of carbonate and phosphate from bone to buffer hydrogen ion. Concomitant mobilization of bone calcium results in hypercalciuria. In addition, metabolic acidosis may induce hypocitrituria. Hypocitrituria may increase the risk for CaOx uroliths because citrate is an inhibitor of CaOx crystal formation.

15. Excessive dietary levels of vitamin D (which promotes intestinal absorption of calcium) and ascorbic acid (a precursor of oxalic acid) should be avoided. The diet should be adequately fortified with vitamin B6 because vitamin B6 deficiency promotes endogenous production and subsequent urinary excretion of oxalic acid.

16. Although increased dietary sodium is associated with increased urinary excretion of calcium, recent studies indicate that calcium concentration may not rise because of a concomitant increase in urine volume. In addition, increased urine volume may decrease urine oxalic acid concentration. Thus, the overall effect of adding sodium chloride to the diet may be increased urine volume and reduced supersaturation with CaOx. Current evidence suggests that restriction of dietary sodium is not of benefit in prevention of CaOx uroliths.

17. Epidemiological studies indicate that cats fed high moisture (canned) diets are three times less likely to develop CaOx uroliths as cats fed low-moisture (dry) diets. High moisture diets are preferred over dry formulations because by promoting increased fluid intake they reduce urinary concentration of calulogenic substances in urine. By increasing urine volume and frequency of voiding, they also minimize the time that crystals can grow by remaining within the urinary tract.

18. Epidemiological studies indicate that cats fed diets with a lower quantity of magnesium had a higher risk for CaOx uroliths than cats fed moderate quantities of magnesium. However, supplemental magnesium may contribute to hypercalciuria, and may also increase the risk for struvite urolith formation. Pending further studies, we do not recommend dietary magnesium restriction or supplementation to minimize recurrence of CaOx uroliths in cats.

19 Epidemiological studies indicate that diets high in potassium were associated with a decreased risk for CaOx uroliths. Studies in humans suggest that oral potassium supplements may reduce urinary excretion of calcium. In addition, oxalic acid forms salts with potassium that are more soluble than CaOx.

Dietary recommendations

1. The goals of dietary prevention include:

• reducing calcium concentration in urine,
• reducing oxalate concentration in urine,
• promoting higher concentrations and activity of inhibitors of calcium crystal growth and aggregation, and
• reducing urine concentration and minimizing urine retention.

2. Results of epidemiological studies in humans, dogs and cats indicate CaOx urolith recurrence may be minimized by feeding a nonacidifying, high-moisture diet formulated to avoid excessive protein, calcium, oxalate and sodium. The diet should contain adequate quantities of phosphorus so as to minimize renal activation of vitamin D, adequate quantities of magnesium, adequate quantities of potassium, and adequate quantities of vitamin B6.

3. Increased water intake is the cornerstone of therapy to prevent urolith recurrence.

High-moisture diets are preferred over dry formulations because by promoting increased fluid intake they reduce urinary concentration of calulogenic substances in urine. By increasing urine volume and frequency of voiding, they also minimize the time that crystals can grow by remaining within the urinary tract. The goal is to promote urine with a specific gravity value ≤ 1.025. Alternatively, water or other liquids may be added to the patient’s usual diet. Living conditions should be adjusted so that the frequency of micturition is not restricted.

4. It is unlikely that water hardness plays a significant role in the formation of uroliths. The quantity of water consumed is much more important. Therefore, use of distilled water is of questionable value, unless it can be documented that it enhances a patient's water consumption and urine volume.

5. As with calcium supplements given independently of the diet, vitamin C and D supplements are not recommended.

Pharmacologic recommendations

1. Detection of persistent calcium oxalate crystalluria or recurrence of uroliths may prompt consideration of other therapeutic strategies. Before considering adding drugs to the prevention protocol, appropriate consideration should be given to owner and patient compliance with dietary recommendations.