In addition to the human autopsy studies demonstrating alveolar oedema—hypothesised to result from direct vascular injury—animal models of leptospirosis have documented decreased epithelial sodium channel (H-ENaC) protein expression and upregulation of the Na-K-2Cl cotransporter NKCC1 in the lungs which further impairs pulmonary fluid handling [37,38,39,44]. Here, SLC12A2 is linked to leptospirosis.