Urate Urolithiasis in a Dalmatian 

On 11 July, Charlie, a three year old Dalmatian, presented to Veterinarium for evaluation and treatment. His clinical signs included pollakiuria (frequent urination) and haematuria (blood in the urine), with blood clots also observed.

Charlie’s diagnostic workup and treatment were managed by Mariam Berishvili, an internist at Veterinarium. 

To establish an accurate diagnosis, Charlie underwent a comprehensive diagnostic evaluation, including a complete abdominal ultrasound examination, a complete blood count, serum biochemistry, and urinalysis. All laboratory tests were performed at the Veterinarium laboratory.

Ultrasonography revealed marked thickening of the urinary bladder wall and urolithiasis, with sediment and small calculi present within the bladder. Urinalysis confirmed the presence of urate sediment.

Nearly 100% of Dalmatians carry a mutation in the SLC2A9 gene, which causes hyperuricosuria (HUU). This condition impairs the metabolism of uric acid into allantoin, resulting in the precipitation of urates in the urine and the formation of uroliths (calculi) in the urinary bladder or kidneys.

In addition to genetic predisposition, urate urolithiasis may be associated with a congenital hepatic vascular anomaly known as a portosystemic shunt. In Charlie’s case, serum biochemistry and ultrasonography ruled out hepatic disease, indicating that the condition was associated with his breed related genetic predisposition. Ultrasonography also showed no evidence of nephrolithiasis (kidney stones).

One of the primary goals in treating urolithiasis is the complete removal of calculi and sediment from the urinary bladder. As Charlie’s calculi were small, bladder lavage was performed. Using urinary catheterisation, sterile fluids, and gentle aspiration, the accumulated urate sediment and small calculi were successfully flushed from the bladder.

To reduce the risk of urate recurrence, Charlie was prescribed a specialised therapeutic diet designed to optimise urinary pH and reduce urate formation associated with impaired uric acid metabolism.

Charlie’s clinical signs have already improved, and he continues to receive appropriate treatment