Abstract

Managed bottlenose dolphins are susceptible to ammonium urate (NH₄U) kidney stones.^1-3 The propensity for NH₄U stone formation is due in part to an increase in urinary ammonium (NH₄⁺), uric acid and pH following a large fish meal, creating a favorable urinary environment for the precipitation of the sparingly soluble NH₄U salt.⁴

We tested the hypothesis that dietary fish types will influence urinary physicochemistry and risk factors for kidney stone formation. The acid-ash content and purine composition of various fish types were analyzed to aid in the formulation of a modified diet (50% finger mullet + 25% capelin + 25% mix of herring and squid) targeting a lower acid and lower purine composition. This newly formulated diet was then fed to 6 dolphins (3 with kidney stones, 3 control dolphins) for 6 months. Blood and spot check urine collections (fasting and 2 hr post-prandial) were performed at baseline, 6 weeks, 3 months, and 6 months to evaluate the impact of the modified fish diet on urine physicochemistry and kidney stone risk factors longitudinally.

Comparing baseline urine to 6 weeks post diet modification, the newly formulated diet was associated with a decrease in pre- and post-prandial urinary NH₄⁺, net acid excretion (NAE), and an increase in net GI absorption of alkali (NGIA), culminating with a decrease in urinary supersaturation of NH₄U (SI NH₄U). At 3 months, NH₄⁺ and NAE were unchanged from baseline while NGIA remained increased. No significant changes were noted in NH₄⁺, NAE or NGIA at 6 months of diet modification, however, the marked postprandial increase in baseline SI NH₄U diminished at 6-months. Urinary citrate increased pre-prandially at 6-weeks and 3-months, and post-prandially at 6-months over baseline. Urinary uric acid increased pre-prandially over baseline at 6 months. Urinary phosphorus declined markedly at 6-weeks, 3-months and 6-months of diet modification. Urinary pH, sodium, calcium, magnesium, oxalate and chloride all remained unchanged after diet modification.

These changes in urine physicochemistry demonstrate a dietary impact on the risk factors that may lead to stone formation in dolphins. Further diet investigations are warranted to evaluate these impacts in order to optimize the diet of dolphins under human care.

Acknowledgments

We acknowledge the ONR grant numbers that supported this work (N00014-15-1-2131 & N00014-15-1-2327). The authors also sincerely thank all of the veterinarians, technicians, trainers, and research team members that assisted in acquiring the samples and data for this project.

* Presenting author

Literature Cited

1.  Venn-Watson S, Smith CR, Johnson S, Daniels R, Townsend F. 2010. Clinical relevance of urate nephrolithiasis in bottlenose dolphins Tursiops truncatus. Diseases of Aquatic Organisms. Mar 9 89(2):167–177.

2.  Venn-Watson SK, Townsend FI, Daniels RL, et al. 2010. Hypocitraturia in common bottlenose dolphins (Tursiops truncatus): assessing a potential risk factor for urate nephrolithiasis. Comparative Medicine. 60(2):149–153.

3.  Smith CR, Venn-Watson S, Wells RS, et al. 2013. Comparison of nephrolithiasis prevalence in two bottlenose dolphin (Tursiops truncatus) populations. Frontiers in Endocrinology. 4:145.

4.  Smith CR, Poindexter JR, Meegan JM, et al. 2014. Pathophysiological and physicochemical basis of ammonium urate stone formation in dolphins. The Journal of Urology. 192(1):260–266.