Citation

Chugh KS. Kidney Int. 1989; 35(3): 891-907.

Affiliation

Postgraduate Institute of Medical Education and Research, Chandigarh, India.

Copyright

(Copyright © 1989, Nature Publishing Group)

DOI

unavailable

PMID

2651763

Abstract

Acute renal failure complicates the course in 5% to 30% of victims of severe viper poisoning. No consensus exists on the single mechanism causing acute renal failure after viper bite. It is known, however, that viper venom induces several clinical abnormalities that favor the development of acute renal failure. These alterations include a varying degree of bleeding, hypotension, circulatory collapse, intravascular hemolysis, and disseminated intravascular coagulation with or without microangiopathy. A direct cytotoxic action of snake venom on the kidney is suspected, but convincing evidence is still lacking. Severe hypocomplementemia is consistently present, but I doubt its role in the causation of renal lesions. Hypersensitivity to venomous or antivenomous protein occasionally causes acute renal failure. In sea snake poisoning, myonecrosis and myoglobinuria appear to play the predominant pathogenetic role. The renal lesions of clinical significance in envenomed patients are acute tubular and patchy or diffuse cortical necrosis. Glomerulonephritis, interstitial nephritis, and papillary necrosis have been reported in rare patients. I trust that this overview of the clinical and basic-science aspects of snake-bite-induced acute renal failure will prompt investigators to further define the pathogenetic mechanisms involved. Lessons learned may aid patients with acute renal failure of diverse causes, both here in India and around the world.

Language: en