Calcium oxalate (CaOx) was the most common (47 percent) mineral in feline uroliths submitted to the Minnesota Urolith Center
during 2003 (Table 1). More than two-thirds of feline nephroliths were composed of CaOx.
Medical protocols that will promote dissolution of CaOx uroliths are not yet available. Urocystoliths small enough to pass
through the urethra may be removed with the aid of voiding urohydropropulsion. Surgery is currently the only practical alternative
for removal of larger active CaOx uroliths. In some patients, uroliths may be eliminated with the aid of lithotripsy.
Cats that have formed CaOx uroliths are at substantial risk of stone recurrence within 12 to 24 months. Therefore, medical
protocols should be considered to minimize urolith recurrence. The objective of Part 3 of this series is to provide insight
into the risks and benefits associated with therapeutic strategies designed to prevent recurrence of feline CaOx uroliths.
Therapeutic caveats associated with other types of uroliths will be the subject of future Diagnotes.
1. CaOx urolith formation does not occur as a result of a single cause. Rather it is the result of varying combinations
of risk factors that promote precipitation of calcium and oxalic acid in urine.
2. As clinicians, we think of risk factors and protective factors as events that affect the likelihood of urolithiasis occurring.
There are many types of risk factors, but, in general they may be listed under three categories:
- etiological risk factors such as infections and endocrinopathies,
- demographic risk factors such as breed, age, gender, and
- genetic predisposition, and environmental risk factors such as living conditions and sources of water and food.
3. When used in a qualitative (rather than a quantitative) way, the significance of risk (or protective) factors should not
be assigned an "all or none" or "always or never" interpretation. Each contributing risk factor may play either a limited
or significant role in the development of uroliths. In some situations, individual risk factors may not be a factor in every
exposed patient. Furthermore, identifying one event in a chain of etiologic events is not the same as identifying all components
in the etiologic chain.
4. In general, prevention strategies are designed to eliminate or control risk factors associated with calculogenesis. Exposure
to some risk factors can be eliminated or controlled; others cannot (Table 2, p. 6S). Preventative therapy is especially important
for patients with a large number of persistent risk factors for CaOx uroliths.
5. Epidemiological studies indicate that males (~60 percent) are more commonly affected than females (~40 percent). In one
study, neutered cats were seven times more likely to develop CaOx uroliths than sexually intact cats.
6. Whereas struvite uroliths are more commonly detected in young to middle age cats (2 to 6 years old), the mean age of cats
at the time of detection of calcium oxalate uroliths is ~8 years. However, CaOx uroliths have been detected in cats ranging
in age from less than 1 year to more than 15 years.
7. Epidemiological studies indicate that CaOx uroliths have been observed in most breeds of cats. However, Himalayan, Persian,
Ragdoll, Havana Brown and Scottish Fold cats were at increased risk for CaOx uroliths, while Siamese and Abyssinian cats had
a reduced risk of urolith formation.
8. Hypercalciuria is a major risk factor for CaOx urolith formation. Hypercalciuria may be associated with 1) hypercalcemia,
2) hyperabsorption of calcium from the intestinal tract, 3) impaired renal reabsorption of calcium, and/or, 4) excessive mobilization
of skeletal calcium. Other risk factors that have been associated with calcium oxalate uroliths include acidosis, hyperoxaluria,
hypocitrituria, hypomagnesuria, decreased urinary concentration of crystallization inhibitors and formation of small volumes
of concentrated urine.
9. Empirical clinical observations indicate that mild hypercalcemia may be present in approximately one-third of cats with
CaOx uroliths. Although serum total calcium concentration and blood-ionized calcium have been mildly increased, parathyroid
concentrations have not been elevated. Unfortunately, the underlying cause of hypercalcemia in most of these cats has not
yet been identified. Causes of hypercalcemia excluded in these patients include primary hyperparathyroidism, hypervitaminosis
D and hypercalcemia of malignancy.
10. Intestinal absorption of excessive calcium will result in hypercalciuria. Therefore, it would seem logical that restriction
of dietary calcium would minimize calcium oxalate urolith formation. However, dietary restriction of calcium may actually
increase the risk for CaOx urolith formation. Why? As in the urinary tract, calcium and oxalic acid in the intestinal lumen
may combine to form an insoluble complex that is not absorbed. However, reducing dietary calcium without an appropriate reduction
in oxalate will increase the solubility of unbound oxalic acid in the intestinal lumen This promotes absorption and subsequent
excretion of oxalic acid in urine. Hyperoxaluria is a greater risk factor for CaOx urolith formation than hypercalciuria of
equivalent magnitude because smaller increments of oxalic acid are required for formation of insoluble CaOx. This provides
a plausible explanation as to why calcium oxalate uroliths recur more frequently in humans consuming calcium-restricted diets
compared to those consuming diets with adequate calcium. It follows that the quantity of dietary calcium should not be altered
without considering an appropriate reduction in the quantity of dietary oxalic acid.