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Originally published online as doi:10.2353/ajpath.2007.060984 on June 28, 2007

Published online before print June 28, 2007
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(American Journal of Pathology. 2007;171:402-414.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060984

A Protein Toxin from the Sea Anemone Phyllodiscus semoni Targets the Kidney and Causes a Severe Renal Injury with Predominant Glomerular Endothelial Damage

Masashi Mizuno*{dagger}, Masatoshi Nozaki{ddagger}, Nobuya Morine{ddagger}, Norihiko Suzuki*, Kazuhiro Nishikawa§, B. Paul Morgan{dagger} and Seiichi Matsuo*

From the Department of Nephrology,* Nagoya University Graduate School of Medicine, Nagoya, Japan; the Department of Medical Biochemistry and Immunology,{dagger} School of Medicine, Cardiff University, Cardiff, United Kingdom; the Department of Health Science,{ddagger} Okinawa Prefectural Institute of Health and Environment, Okinawa, Japan; and the Division of Nephrology and Rheumatology,§ Department of Internal Medicine, Aichi Medical University, Aichi, Japan

Envenomation by the sea anemone Phyllodiscus semoni causes fulminant dermatitis and, rarely, acute renal failure in humans. Here, we investigated whether the venom extracted from the nematocysts (PsTX-T) was nephrotoxic when administered intravenously in rats and whether PsTX-T induced activation of the complement system. Although small dose of PsTX-T induced acute tubular necrosis in rats resembling pathology seen in patients, kidneys displayed glomerular injury with glomerular endothelial damage, thrombus formation, mesangiolysis, and partial rupture of glomerular basement membrane, accompanied by severe tubular necrosis at 24 hours after administration of 0.03 mg of PsTX-T per animal, similar to the glomerular findings typical of severe hemolytic uremic syndrome. The early stage injury was accompanied by specific PsTX-T binding, massive complement C3b, and membrane attack complex deposition in glomeruli in the regions of injury and decreased glomerular expression of complement regulators. A pathogenic role for complement was confirmed by demonstrating that systemic complement inhibition reduced renal injury. The isolated nephrotoxic component, a 115-kd protein toxin (PsTX-115), was shown to cause identical renal pathology. The demonstration that PsTX-T and PsTX-115 were highly nephrotoxic acting via induction of complement activation suggests that inhibition of complement might be used to prevent acute renal damage following envenomation by P. semoni.






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Copyright © 2007 by the American Society for Investigative Pathology.