Feline lower urinary tract disease (FLUTD) encompasses a number of clinical disorders that commonly affect cats. The causes of FLUTD are varied and the disease remains poorly understood. The processes involved in the formation of calcium oxalate urolithiasis (CaOx) is an example of this lack of knowledge.

In 1984, a study reported an incidence of CaOx as low as 2-3% of all feline urinary stones (uroliths). The situation today is dramatically different with various studies reporting incidences as high as 54%. Although this shift in incidence is likely due in part to better management of struvite urolithiasis (Struvite stones consist of a mineral complex involving ammonium, magnesium and phosphate and the stones most familiar to cat owners), CaOx is undisputably diagnosed much more frequently.

In cats, CaOx tends to develop in middle aged cats, 4 years and older. Although found in any breed, the Persian is particularly predisposed with Himalayan and Burmese over-represented to a lesser extent. In some studies, the Siamese has been under-represented. Gender does not appear to be a factor, although a greater incidence occurs in sterilized cats. Cats receiving products that acidify the urine are also predisposed. Additional factors may also include exclusive feeding of a single brand of cat food and maintaining cats in an indoor environment. Indoor cats presumably void less frequently allowing the components of bladder stones a longer period of time to precipitate if in a supersaturated state.

In order for a urolith to form, urine must have a high concentration (supersaturation) of the individual mineral components that can form the stone. With respect to CaOx, two opposing factors interplay the presence of calcium and oxalate in sufficient high urinary concentrations to be supersaturated, and the presence of so-called crystallization inhibitors (ie. Compounds that help prevent the formation of CaOx stones), such as magnesium, citrate and sodium.

Some cats with a genetic deficiency in an enzyme called D-glycerate dehydrogenase, a liver enzyme responsible for breaking down precursors of oxalic acid, have been found to form CaOx stones much more readily than normal cats. However, the likelihood that this deficiency plays a role in the formation of CaOx in the general cat population is unlikely.

During the past 10-15 years, feline diets have undergone significant reformulations by manufacturers with a tendency to acidify urine to help prevent struvite urolithiasis. Formulating cat foods to produce acidic urine also results in more calcium (one of the two components of CaOx) being found in the urine. This increased concentration of calcium resulted from more calcium being absorbed from the bones into the bloodstream and excreted by the kidneys into the urine.

One study, however, has indicated that acidifying the diet alone may not be enough to predispose to CaOx formation. The greatest supersaturation of calcium oxalate (and hence the tendency for CaOx stones to form) was found to occur not simply with the lowest pH urine, but rather when the urine was both acidic and restricted in magnesium concentration. Similarly, numerous studies have shown that feeding magnesium restricted diets in cats enhanced the formation of CaOx. In man, magnesium supplements decrease the formation of CaOx. Hence the restriction of magnesium in urine acidifying cat foods (a common practice by pet food manufacturers to help prevent struvite stones) implies a strong role for magnesium in CaOx formation. The exact means by which magnesium may have this inhibitory role is unknown.

Research in man and other species has indicated that increased amounts of animal protein significantly increase urinary excretion of calcium and oxalate. If the same process occurs in cats, then an emphasis on a diet with less animal protein, yet still nutritionally balanced, might be helpful in avoiding reoccurrence of CaOx.

Several studies have examined the relevance of dietary water content in the formation of uroliths, with inconclusive results. With the intent of enhancing the passage of large amounts of urine and maximizing urine turnover time, it would seem appropriate to encourage highly digestible foods with high moisture content.

Since the processes involved in CaOx formation in cats remain poorly understood, it is difficult for veterinarians to make firm recommendations to their clients to help prevent reoccurrences. Avoiding a single diet should be considered, as should diets that do not acidify urine, nor are restricted in magnesium content. Excessive levels of Vitamin D (which will increase intestinal absorption of calcium) and ascorbic acid (a precursor of oxalate) are also best avoided.