Etiopathogenesis of uric acid and ammonium urate uroliths in non-Dalmatian dogs.

The etiopathogenesis of uric acid, sodium acid urate, and ammonium acid urate uroliths in non-Dalmatian dogs appears to be a complex phenomenon. It may involve one or more pathologic and/or physiologic processes acting independently or in concert to increase urinary concentration of lithogenic substances that result in initiation, growth, and retention of urate uroliths. Increased urine uric acid concentration and/or urinary excretion of uric acid appear to be primary predisposing factors in urate lithogenesis. Specific disorders resulting in hyperuricuria may involve abnormalities of increased synthesis, diminished biodegradation, and/or enhance excretion of uric acid. In addition, ammonium ion, hydrogen ion, and other organic and inorganic urine constituents appear to have major influences on urate urolith formation. Unfortunately, many specific disorders of uric acid metabolism and other factors promoting or inhibiting urate urolith formation remain poorly characterized in the majority of non-Dalmatian dogs with urate urolithiasis. Growing awareness of the significance of urate uroliths in non-Dalmatian dogs should encourage further investigation into the identification, characterization, and quantitation of parameters influencing urate lithogenesis. Results of such studies are required for development of practical and effective strategies for treatment and prevention of canine urate urolithiasis.