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Pathophysiological effects of Russell's viper venom on renal function
1Department of Physiology, Faculty of Veterinary Science, Chulalongkorn University, Queen Saovabha Memorial Institute, Bangkok, Thailand.
Journal of Natural Toxins
|December 11, 1999
Summary
Russell's viper venom (RVV) causes significant cardiovascular and renal hemodynamic changes in experimental animals. RVV directly impacts renal tubular cells, leading to impaired kidney function long after envenomation.
Area of Science:
- Toxicology
- Nephrology
- Cardiovascular Physiology
Background:
- Russell's viper venom (RVV) envenomation presents complex pathophysiological challenges.
- Understanding RVV's impact on renal function is crucial for effective treatment strategies.
Purpose of the Study:
- To review the pathophysiological effects of RVV on renal function.
- To explore the mechanisms of RVV action on renal hemodynamics and tubular cells in experimental models.
Main Methods:
- Review of experimental animal studies investigating RVV effects.
- Analysis of cardiovascular and renal hemodynamic parameters post-envenomation.
- Examination of in vitro data on RVV's direct effects on renal tubular cells.
Main Results:
- RVV initially decreases mean arterial blood pressure, heart rate, cardiac output, and renal hemodynamics, while increasing vascular resistance.
- While general circulation parameters normalize within 30 minutes, renal vasoconstriction, reduced renal blood flow, and decreased glomerular filtration rate persist for at least 48 hours.
- RVV directly affects renal tubular cells, impacting cell membrane polarization, mitochondrial activity, and Na, K-ATPase activity.
Conclusions:
- RVV induces significant and prolonged renal hemodynamic disturbances.
- Direct cellular toxicity of RVV on renal tubules contributes to nephrotoxicity.
- Further research into humoral factors and cellular mechanisms is warranted to mitigate RVV-induced kidney damage.