Renal dysfunction by scorpion toxins is caused by renal
ischemia induced by intense renal vasoconstriction due to
catecholamines, angiotensin II and effects of venom on
vascular ion channels. Effects of proinflammatory cytokines,
venom enzymes and inflammatory reactions are
equally important contributions to the development of
acute renal injury. Serum electrolyte changes in scorpionism
can be nonspecific secondary to either gastrointestinal
disturbance caused by parasympathetic stimulation or
acute renal failure. However, the specific effect of scorpion
venom on inhibition of K transport of renal tubular K
secretory channels (Kv, ROMK and Kca) can cause K
retention and hyperkalemia which stimulates aldosterone
secretion. Hyperaldosteronism as a secondary effect of the
venom through the host response stimulates K secretion by
ROMK2 and ROMK3 spared from venom inhibition and
causes hypokalemia. The venom effects thus counteract
each other and the serum K is the net result of the two
effects taking also in consideration K intake and the presence
of ACEI in some scorpion species. Hyperkalemia in
scorpion envenoming is therefore inconsistent. Scorpionism
is a good lesson for exercise in renal physiology