Electrolyte imbalances that can be triggered by Kambô use include hypokalemia, hypomagnesemia, hypophosphatemia, and most concerningly, hyponatremia, which arise neurophysiologically through peptide-induced activation of gastrointestinal and autonomic pathways, specifically via CCK-A and NK1 receptor stimulation, leading to intense vomiting, diarrhea, and salivary losses, compounded by sauvagine-driven CRF1 receptor activation, which can provoke non-osmotic ADH release and SIADH, impairing renal free water clearance and promoting dilutional electrolyte disturbances [8,9]. Here, CCKAR is linked to familial primary hypomagnesemia.