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Journal of Wildlife Diseases, 41(4), 2005, pp. 707-716
© Wildlife Disease Association  2005
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PATHOLOGY AND PROPOSED PATHOPHYSIOLOGY OF DICLOFENAC POISONING IN FREE-LIVING AND EXPERIMENTALLY EXPOSED ORIENTAL WHITE-BACKED VULTURES (GYPS BENGALENSIS)

Carol Uphoff Meteyer1,7, Bruce A. Rideout2, Martin Gilbert3,6, H. L. Shivaprasad4 and J. Lindsay Oaks5

1 USGS National Wildlife Health Center, 6006 Schroeder Rd., Madison, Wisconsin 53711, USA
2 Center for Reproduction of Endangered Species, Zoological Society of San Diego, PO Box 120551, San Diego, California 92112, USA
3 The Peregrine Fund, 5668 West Flying Hawk Lane, Boise, Idaho 83709, USA
4 California Animal Health and Food Safety Laboratory System-Fresno Branch, University of California at Davis, 2789 S Orange Avenue, Fresno, California 93725, USA
5 Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 99164-7040, USA
7 Corresponding author (email: carol_meteyer{at}usgs.gov)

ABSTRACT:   Oriental white-backed vultures (Gyps bengalensis; OWBVs) died of renal failure when they ingested diclofenac, a nonsteroidal anti-inflammatory drug (NSAID), in tissues of domestic livestock. Acute necrosis of proximal convoluted tubules in these vultures was severe. Glomeruli, distal convoluted tubules, and collecting tubules were relatively spared in the vultures that had early lesions. In most vultures, however, lesions became extensive with large urate aggregates obscuring renal architecture. Inflammation was minimal. Extensive urate precipitation on the surface and within organ parenchyma (visceral gout) was consistently found in vultures with renal failure. Very little is known about the physiologic effect of NSAIDs in birds. Research in mammals has shown that diclofenac inhibits formation of prostaglandins. We propose that the mechanism by which diclofenac induces renal failure in the OWBV is through the inhibition of the modulating effect of prostaglandin on angiotensin II-mediated adrenergic stimulation. Renal portal valves open in response to adrenergic stimulation, redirecting portal blood to the caudal vena cava and bypassing the kidney. If diclofenac removes a modulating effect of prostaglandins on the renal portal valves, indiscriminant activation of these valves would redirect the primary nutrient blood supply away from the renal cortex. Resulting ischemic necrosis of the cortical proximal convoluted tubules would be consistent with our histologic findings in these OWBVs.
  Key words:  Diclofenac, Gyps bengalensis, nonsteroidal anti-inflammatory drugs, Oriental white-backed vulture, pharmaceutical residues, renal portal system, renal tubule necrosis, visceral gout.

6 Current address: The Wildlife Conservation Society Field Veterinary Program in Phnom Penh, Cambodia






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