ArticlePLoS neglected tropical diseases2011
Loxosceles gaucho venom-induced acute kidney injury--in vivo and in vitro studies.
Article in PLoS neglected tropical diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Comparative treatment with hyperbaric oxygen therapy in a model of systemic loxoscelism in rats.Iranian journal of basic medical sciences · 2022Article
- Protective Effectiveness of an Immunization Protocol Against the Toxic Effects ofFrontiers in veterinary science · 2022Article
- Brown spider venom toxins: what are the functions of astacins, serine proteases, hyaluronidases, allergens, TCTP, serpins and knottins?The journal of venomous animals and toxins including tropical diseases · 2021Article
- EPILAT-IRA Study: A contribution to the understanding of the epidemiology of acute kidney injury in Latin America.PloS one · 2019Observational
- Article
- Highlights in the knowledge of brown spider toxins.The journal of venomous animals and toxins including tropical diseases · 2017Review
- A novel hyaluronidase from brown spider (Loxosceles intermedia) venom (Dietrich's Hyaluronidase): from cloning to functional characterization.PLoS neglected tropical diseases · 2013Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccidents caused by Loxosceles spider may cause severe systemic reactions, including acute kidney injury (AKI). There are few experimental studies assessing Loxosceles venom effects on kidney function in vivo. METHODOLOGY/PRINCIPAL
findingsIn order to test Loxosceles gaucho venom (LV) nephrotoxicity and to assess some of the possible mechanisms of renal injury, rats were studied up to 60 minutes after LV 0.24 mg/kg or saline IV injection (control). LV caused a sharp and significant drop in glomerular filtration rate, renal blood flow and urinary output and increased renal vascular resistance, without changing blood pressure. Venom infusion increased significantly serum creatine kinase and aspartate aminotransferase. In the LV group renal histology analysis found acute epithelial tubular cells degenerative changes, presence of cell debris and detached epithelial cells in tubular lumen without glomerular or vascular changes. Immunohistochemistry disclosed renal deposition of myoglobin and hemoglobin. LV did not cause injury to a suspension of fresh proximal tubules isolated from rats. CONCLUSIONS/SIGNIFICANCE: Loxosceles gaucho venom injection caused early AKI, which occurred without blood pressure variation. Changes in glomerular function occurred likely due to renal vasoconstriction and rhabdomyolysis. Direct nephrotoxicity could not be demonstrated in vitro. The development of a consistent model of Loxosceles venom-induced AKI and a better understanding of the mechanisms involved in the renal injury may allow more efficient ways to prevent or attenuate the systemic injury after Loxosceles bite.
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