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.