THE dog that walks into your next consult is not quite the picture of an incontinence case that you expected when quickly glancing at the morning’s diary.
“Jed” is a six-year-old neutered male Cocker spaniel who presents to you as what you might say is a “typical” urinary case.
“He’s never been a big drinker,” his owners say, but their concern now is the frequency with which he now “dribbles” on the rug when they’re not conscientious about leaving the door open for his outside access.
Given your colleague (the ultrasonographer extraordinaire) is just finishing up a scan, you coax her (with biscuits and tea) into putting the probe on Jed for a while as you look at the urine sample the owners have dutifully brought in.
On the microscope you find quite a bit of sediment with some crystals that you don’t recognise and, in the next room, she finds quite a sizeable stone in the bladder. This urine, which is ++ blood on dipstick, will need to go to the lab of course.
Given the options, Jed’s owner is set on surgical removal, alongside the antibiotic cover you’re confident in prescribing after taking another decent urinary sample for culture and sensitivity.
You go ahead after collecting your minimum database (bloods on top of the UA already requested) and remove a 1.5cm diameter light-brown roughsurfaced stone from the bladder.
While you recall that 80-90% of stones are struvite and oxalate, you’re convinced that this one is otherwise, given those crystals and urine pH is already quite low. It’s a case of urate stones, as confirmed by urolith analysis which reports 95% ammonium urate with a struvite/oxalate band.
So what’s happening with Jed? What combination of events have led to this stone and how can we be confident we’re doing all that we can for this Cocker and his owner?
Urate stones are the result of abnormalities in dealing with uric acid. There are a number of predisposing factors and trends in diagnosis with these stones (males>females, over-represented breeds including Dalmatian, English Bulldog, and Miniature Schnauzer, acidic urine) but at the end of the day it’s hyperuricosuria (excess uric acid in the urine) which needs addressing.
The liver and the processing of the metabolic products of purines (originating endogenously from DNA nucleotides and certain proteins in the diet) are central to this process.
Purine breakdown is a multi-step process. The first step produces xanthine which is oxidised to yield uric acid. In the healthy pet, hepatic uricase converts most of this one final step to allantoin, a highly soluble molecule which is then eliminated via the urine. The ratio of uric acid to allantoin in “healthy” urine is very much in favour of the latter solute, meaning there’s a low risk of urate urolithiasis.
When things go wrong, a mutation (common in predisposed breeds including the Dalmatian) leads to defective transport of uric acid across the liver cell membrane. For this reason uric acid isn’t converted to allantoin so effectively and, additionally, there is a lower resorption of uric acid at the proximal renal tubule. This means that the urine becomes saturated with uric acid which most commonly crystallises with ammonium in the higher urinary pH ranges.
This atypical processing of purine metabolites not only happens in those with a genetic mutation but is seen in individuals (mainly dogs) with hepatic dysfunction, particularly those with vascular anomalies such as portosystemic-shunts.
Along with his clinical signs, the bloods you’ve collected from Jed don’t suggest a hepatic issue at all so in this instance we’re looking at a break in that chain of dealing with uric acid.
You note also that, on a previous visit, Jed’s owner admits to feeding tripe which is on your list of high uric acid foodstuffs which could contribute to the relative acidity of his urine as well as giving the body a good old dose of purine which will challenge those hepatic metabolic pathways.
To manage him on an ongoing basis we’d like to ensure the lowest chances of stone recurrence. This may include the use of allopurinol (xanthine oxidase inhibitor) and steps in urinary alkalinisation, but eliminating purines from the equation via diet is central to achieving our goal.
Prompted by your nurse (always good with nutrition) you’re able to find one of the clinical diets developed specifically for the management of dogs with urate stones. These diets are traditionally protein restricted (with protein accounting for 8-10% of total calories) but the use of low-purine protein sources (of non-meat origin) can help us reduce purine intake too.
We should always be mindful to avoid feeding low-protein diets to dogs in growth or in situations of high basal requirements (malnutrition, burns, peritonitis, wound healing and protein-losing conditions); however, if we select our protein sources wisely, we can provide sufficient levels in a formula to allow long-term maintenance feeding of the diet.
Coupled with the inclusion of urine alkalinisers such as potassium citrate, ammonium urate precipitation is markedly less likely.
As ever (and discussed in last month’s article) we can do Jed a great favour in increasing the water turnover and urine volume travelling through his bladder. A great target to have in mind is bringing the USG below 1.020 in dogs, diluting the urine and in effect reducing the likelihood and time over which solutes can come together, crystallise and precipitate as either crystals or stones.
Jed proves to us that all cases of urolithiasis are not the same. Sometimes we’ll be challenged with mixed, atypical or metabolic stones which encourage us to slow down, review pathophysiology and the factors which have led the patient to our consultation room.
While we could have gone down a dissolution route with Jed, removing that stone is always going to be a good idea. He’s a classic case which we might discuss on the Royal Canin nutritional helpline and it’s always reassuring to know that even atypical stones are manageable given the right tools.
References and further reading
1. Caney, S., Cortadellas, O., Dhumeaux, M. and Nickel, R. (2014) Practical Management of Urinary Tract Disease. Veterinary Focus special edition: Royal Canin, Aimargues France.
2. Hesse, A. and Neiger, R. (2009) A Colour Handbook of Urinary Stones in Small Animal Medicine: Manson Publishing, London.
3. Villaverde, C. (2014) Urates in bladder disease. Veterinary Focus; Lower Urinary Tract Disease 24 (1): 10-14.
