2015 New Treatments, Environmental Triggers, Skin, Human Lupus Biology
2015 Can Reducing Dietary Salt Alleviate Lupus Symptoms?
The Study and What it Means to Patients
Our team has developed an innovative way to use MRI imaging technology to measure salt levels in body tissues, such as skin and muscle. With this technology, we will examine for the first time if lupus patients have excess salt in their tissues and if reducing dietary salt can reduce inflammation and high blood pressure in lupus.
Too much salt in the diet has been linked to high blood pressure and inflammation in the general population. Although high blood pressure is common in lupus, even in patients without lupus nephritis, little is known about the role that salt plays in either causing high blood pressure or inflammation in lupus. Our LRI-funded research will use magnetic resonance imaging (MRI) technology that we developed to measure tissue salt levels in patients with lupus and determine if high tissue salt levels increase inflammation and/or blood pressure. By understanding this correlation, we hope to discover that something as simple as decreasing salt intake may both improve blood pressure and relieve some lupus symptoms.
Scientific Abstract: Tissue sodium in autoimmune disease
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.