Hypocitraturia: A Potential Risk Factor for Nephrolithiasis in Bottlenose Dolphins
IAAAM 2010
Stephanie Venn-Watson1; Forrest I. Townsend2; Risa Daniels1; Jay Sweeney3; Jim McBain4; Leigh Klatsky3; Christie Hicks5; Lydia Staggs6; Teri Rowles7; Lori Schwacke8; Randall S. Wells9; Cynthia R. Smith1
1National Marine Mammal Foundation, San Diego, CA, USA; 2Bayside Hospital for Animals, Fort Walton Beach, FL, USA; 3Dolphin Quest Oahu, Honolulu, HI, USA; 4SeaWorld San Diego, San Diego, CA, USA; 5The Mirage Hotel and Casino, Las Vegas, NV, USA; 6Gulf World Marine Park, Panama City Beach, FL, USA; 7National Marine Fisheries Service, Silver Spring, MD, USA; 8National Ocean Service, Center for Human Health Risks, Charleston, SC, USA; 9Chicago Zoological Society, c/o Mote Marine Laboratory, Sarasota, FL, USA

Abstract

Numerous cases of urate nephrolithiasis have been reported in managed collections of common bottlenose dolphins (Tursiops truncatus), and it is believed that nephrolithiasis is uncommon in wild dolphins.2 Risk factors for urate nephrolithiasis in humans include low urinary pH and hypocitraturia. Urine samples from 94 bottlenose dolphins were collected during April 2006 through June 2009 from four wild populations and four managed collections (managed collection dolphins, n=32; wild dolphins, n=62).1 All samples were tested for urinary creatinine and citrate concentrations. Urinary uric acid and pH were tested in a smaller subset of animals. Our null hypothesis was that there would be no significant differences in urinary creatinine, citrate, and uric acid concentrations and pH among wild and managed collection dolphins. Among urine samples from all 94 dolphins, the mean ± SEM urinary levels for creatinine, citrate, uric acid, and pH were 139 ± 7.6 mg/dl, 100 ± 20 mg citrate/g creatinine, 305 ± 32 mg uric acid/g creatinine, and 6.2 ± 0.05, respectively. Of the four urinary variables, only citrate concentration varied significantly between the two primary study groups; managed collection dolphins were more likely to have undetectable levels of citrate in the urine compared to wild dolphins (81.3% and 21%, respectively; P < 0.0001). Mean urinary citrate concentrations for managed collection and wild dolphin populations were 2 and 150 mg citrate/g creatinine, respectively (P =0.0003). We conclude that some managed collections of dolphins, like humans, may be predisposed to urate nephrolithiasis due to the presence of hypocitraturia. Follow on investigations could include associations between metabolic syndrome, hypocitraturia, and urate nephrolithiasis in humans and dolphins; and the impact of varying levels of seawater ingestion on citrate excretion.

Acknowledgments

The authors thank NMFS Marine Mammal Health and Stranding Response Program and NOAA Oceans and Human Health Initiative for funding the capture-release sampling of wild dolphins. The authors also thank Dr. Greg Bossart the permit holder for the Indian River Lagoon dolphin population study, Larry Hansen for providing animal samples and data, and Dr. Bill Van Bonn for his early investigations related to dolphins and urinary citrate.

References

1.  Venn-Watson S, Townsend FI, Daniels R, Sweeney J, McBain J, Klatsky L, Hicks C, Staggs L, Rowles T, Schwacke L, Wells RS, Smith CR 2010. Hypocitraturia in common bottlenose dolphins (Tursiops truncatus): Assessing a potential risk factor for urate nephrolithiasis. Comp Med 60:1-5.

2.  Venn-Watson S, Smith CR, Johnson S, Daniels R, Townsend F 2010. Clinical relevance of urate nephrolithiasis in bottlenose dolphins (Tursiops truncatus). Dis Aquat Org 89:167-177.

 

Speaker Information
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Stephanie Venn-Watson
National Marine Mammal Foundation
San Diego, CA, USA


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