Citation

Braga JRM, Jorge ARC, Marinho AD, de Moraes Silveira JA, Nogueira-Junior FA, Valle MB, Alagón A, de Menezes RRPPB, Martins AMC, Feijão LX, Monteiro HSA, Jorge RJB. Toxicon 2020; ePub(ePub): ePub.

Affiliation

Federal University of Ceará (UFC), Department of Physiology and Pharmacology, Brazil. Electronic address: robertajeane@ufc.br.

Copyright

(Copyright © 2020, Elsevier Publishing)

DOI

10.1016/j.toxicon.2020.04.095

PMID

32339535

Abstract

The Micrurus snake venoms mainly cause systemic complications, essentially neurotoxicity. Previous studies, however, have described that they are involved in the occurrence of acute kidney injury (AKI) in animal models. AKI pathogenesis in snakebites is multifactorial and involves immunological reactions, hemodynamic disturbances, and direct nephrotoxicity. The aim of this study was to compare the nephrotoxic effects of coral snake venoms from M. browni (MbV) and M. laticollaris (MlV) on the proximal tubular epithelial cell line (LLC-MK2) and isolated perfused kidney. Using an MTT assay, both venoms significantly reduced cell viability at higher concentrations (25-100 μg/mL). MlV (10 μg/mL) increased the perfusion pressure (PP) at 60, 90 and 120 min, while the MbV did it only at 90 and 120 min. Renal vascular resistance (RVR) decreased at 60 min and increased at 120 min with MbV, but decreased at 60, 90 and 120 min with MlV. Urinary flow (UF) alterations were not observed with MlV, but MbV elevated them at 90 and 120 min. Both venoms significantly decreased the glomerular filtration rate (GFR), %TNa⁺, %TK⁺ and %TCl^- levels as of 60 min of perfusion. Oxidative stress analysis revealed that both venoms behaved similarly, reducing glutathione and increasing malondialdehyde levels. Kidney injury is not usually described in clinical cases of Micrurus snakebites. However, the potential for nephrotoxicity should be considered in the overall picture of envenomation.

Copyright © 2020. Published by Elsevier Ltd.

Language: en

Keywords

Acute kidney injury; Coral snake; Cytotoxicity; Kidney perfusion