Salt-sensitive hypertension (SSHT) is commonly framed as a disorder of renal sodium transport and vascular dysfunction. Yet increasing evidence indicates that immune cells also detect sodium excess and convert it into inflammatory signaling. In this article, we argue that the serum and glucocorticoid-regulated kinase 1 (SGK1)/epithelial sodium channel (ENaC) immune axis provides a useful framework for linking salt exposure to renal injury. In antigen-presenting cells (APCs), high salt activates SGK1, increases ENaC expression and sodium entry, and promotes oxidative stress, isolevuglandin formation, inflammasome activation, and cytokine release. In T-lymphocytes (T-cells), SGK1 supports pathogenic effector responses and contributes to hypertensive end-organ inflammation. Together, these observations suggest that immune sodium sensing is not merely a consequence of elevated blood pressure but an active process that sustains renal inflammation and maladaptive remodeling. We further propose that this pathway may help explain how immune-tubular crosstalk amplifies kidney injury in salt-sensitive hypertension. Defining when and where SGK1/ENaC signaling operates across renal immune cell subsets may open new opportunities for targeted therapy.