Protocols have been developed to promote dissolution of canine and feline struvite uroliths, the dissolution of canine ammonium
urate and cystine uroliths, and the prevention of all major types of canine and feline uroliths. However, because the underlying
causes of different types of uroliths vary, medical protocols that promote their dissolution and prevention vary.
The objective of the first article in this two-part series is to summarize diagnostic caveats derived from our experience
with medical management of urolithiasis during the past 25 years.
When the diagnosis of the underlying causes of urolith formation becomes the rule rather than the exception, therapeutic failures
will become the exception rather than the rule. Therapeutic caveats will follow in next month's Diagnotes.
1. Uroliths are always the sequela of one or more underlying inherited, congenital, and/or acquired disorders. Therefore,
detection of uroliths should not be accepted as an endpoint of diagnostic investigation.
2. Although some types of uroliths occur with greater frequency in some species and breeds, breed predisposition should not
be used as primary criteria for diagnosis of the mineral composition of uroliths. For example, of 9,541 uroliths formed by
Dalmatian dogs and submitted to the Minnesota Urolith Center, 9,095 were composed of urates. However, 185 were of mixed composition,
155 were compound stones, 43 were struvite, 21 were composed of calcium oxalate, four were composed of silica, three were
composed of cystine and three were composed of calcium phosphate.
3. Urocystoliths and urethroliths that occur in immature dogs and cats are usually composed of struvite caused by infections
with urease producing microbes (especially staphylococci). Metabolic uroliths (such as calcium oxalate and cystine uroliths)
are uncommonly encountered in immature patients. Two notable exceptions to this generality are the formation of ammonium urate
uroliths in dogs with portovascular anomalies, and formation of cystine uroliths by Newfoundlands.
4. Most feline nephroliths are composed of calcium salts (calcium oxalate or calcium phosphate). Calcium containing nephroliths
are being recognized with increased frequency in cats with chronic renal failure. Only about 5 percent of feline nephroliths
5. Palpation of the urethra (including palpation per rectum) should routinely be performed in patients suspected of having
6. Most (~90 percent) urocystoliths in cats cannot be detected by abdominal palpation. Radiographic or ultrasonographic evaluation
of the urinary tract is required to detect them consistently.
7. It may be impossible to palpate urocystoliths in a patient with a distended or overdistended urinary bladder. The urinary
bladder should be palpated after urine has been eliminated by (depending on circumstances) voiding, manual compression, cystocentesis
8. Detection of crystals in urine is proof that the urine sample is oversaturated with crystallogenic substances. However,
in vitro oversaturation may occur in addition to, or instead of, in vivo events. Therefore, care must be used not to over-interpret
the significance of crystalluria. In vitro crystal formation may have no clinical relevance to in vivo formation of crystals.
9. Change in temperature associated with preservation of urine by refrigeration is a common cause of in vitro crystalluria.
Therefore, presence of crystals in stored samples should be validated by reevaluation of fresh urine.
10. In vitro changes in urine pH also cause changes in crystalluria. When substantial time is expected to lapse between the
urine collection and urine analysis, urine pH values should be obtained immediately following collection and again at the
time of the analysis. Differences between the two pH values suggest that in-vitro changes have occurred, and should be considered
when interpreting the significance of crystalluria. This is especially important when sending samples to diagnostic laboratories.
11. Urine pH values obtained by strips (colorimetric dyes) may vary by as much as 0.5 unit on either side of the observed
value. This variation is associated with logarithmic changes in hydrogen ion concentration. Therefore, when precise urine
pH values are needed, they should be obtained with the aid of a portable pH meter.
12. Urine samples collected and submitted by clients are often unreliable because unknown variables including contamination,
temperature and length of storage, and changes in urine pH may result in formation or dissolution of crystals after sample
13. Consider the patient's diet when interpreting the significance of crystalluria because crystalluria may also be influenced
by diet (including water intake). Dietary influence on crystalluria is of diagnostic importance because urine crystal formation
that occurs while patients are consuming hospital diets may be dissimilar to urine crystal formation that occurs when patients
are consuming diets fed at home.
14. Struvite crystals are often observed when urine pH is slightly acid (6.5) or alkaline. They are unlikely to be observed
when urine pH is - 6.3.
15. Urine sediment should be observed for a tendency of crystal aggregation in addition to crystal type. Crystals that aggregate
in vivo represent a greater risk for urolith formation than single crystals.
16. Detection of unusual crystals in the urine of patients receiving medications should prompt consideration that they may
be drug metabolites. Drug associated crystalluria in dogs and cats includes sulfadiazine and its metabolites.
17. Characterization of amorphous (i.e. without shape) crystals is especially difficult. Calcium phosphate may form amorphous
crystals in alkaline urine; ammonium urate and xanthine may form amorphous crystals in acid urine. Other types of crystals
may also be amorphous. Addition of 10 percent acetic acid usually results in dissolution of calcium phosphate crystals and
often results in formation of characteristic diamond or rhomboid shaped uric acid crystals from amorphous urate crystals.