Vascular dysfunction, and consequently hypertension, are prevalent in SLE and contribute to adverse outcomes. Although high salt intake is strongly associated with vascular dysfunction in the general population, the biology of salt in SLE is not known. We have made three observations that have fundamentally revised our understanding of the biology of salt. First, large amounts of sodium are stored in the skin and these can be quantified in humans using 23Na magnetic resonance imaging. Second, skin sodium concentrations are associated with hypertension, particularly resistant hypertension. Third, sodium drives autoimmune disease by induction of pathogenic TH17 cells in animal models. There is no information about tissue sodium concentrations in SLE. Thus, we will for the first time: 1) quantify tissue sodium concentrations in SLE and define their relationship with vascular function and inflammation; 2) examine the effect of decreased dietary sodium intake on tissue sodium concentrations, vascular function, and inflammation in SLE. We hypothesize that tissue sodium concentrations will be increased and associated with vascular dysfunction and inflammation in SLE, and that reduced dietary sodium intake will ameliorate these effects. These studies have high potential impact by translating advances in biology to improved patient care in SLE.