Hyponatremia could mediate PRES either directly by increased BBB permeability and vascular reactivity due to osmotic factors, or indirectly by elevated ADH via increased secretion of VEGF, accelerated transcription of aquaporin 4 in astrocytes, or activation of vasopressin V1a receptors disturbing cerebral vascular reactivity [63–65]. This evidence concerns the gene AVPR1A and Posterior Leukoencephalopathy Syndrome.