Scorpion venoms, kidney and potassium

Toxicon. 2013 Oct:73:81-7. doi: 10.1016/j.toxicon.2013.06.023. Epub 2013 Jul 5.

Abstract

Scorpion venoms cause renal injury by the interaction of renal ischemia due to intense renal vasoconstriction and inflammatory reactions due to proinflammatory cytokines and mediators. Renal vasoconstriction is not only induced by catecholamine storm but also by angiotensin II and the direct action of venom on vascular ion channels. Increased aldosterone also contributes to hypertension. Blocking of renal tubular K channels decreases renal K excretion and increases serum K level which increases aldosterone release. Hyperaldosteronism increases K excretion mostly through ROMK2 and ROMK3 unblocked by the venom. The presence of angiotensin converting enzyme inhibitor in some scorpion species can increase serum K. Therefore, there are both K increasing and K decreasing effects in renal K excretion. Serum K in scorpionism is the net result of the two opposing effects. Hyperkalemia is therefore inconsistent.

Keywords: Renal K Channels; Renal injury; Scorpion toxins; Serum K.

Publication types

  • Review

MeSH terms

  • Humans
  • Ischemia / chemically induced*
  • Kidney / blood supply*
  • Kidney / drug effects*
  • Potassium / blood*
  • Potassium Channels / metabolism*
  • Scorpion Stings / blood
  • Scorpion Stings / physiopathology*
  • Scorpion Venoms / toxicity*
  • Vasoconstriction / drug effects*

Substances

  • Potassium Channels
  • Scorpion Venoms
  • Potassium