Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that predominantly affects women during their reproductive years. Although SLE can affect any organ system, the kidneys are prominently involved in the form of immune complex glomerulonephritis. In addition, women with SLE have a dramatically increased risk for the development of cardiovascular disease. Hypertension is a major risk factor for cardiovascular disease and is highly prevalent in women with SLE. Despite this, little has been explored regarding the pathophysiological mechanisms that promote SLE hypertension. This review discusses the role of several mechanisms, with an emphasis on the kidney, may contribute to SLE hypertension. These include the renin-angiotensin system, endothelin, oxidative stress, sex steroids, metabolic changes, peroxisome proliferator activated receptor gamma, and perhaps most importantly, chronic inflammation and cytokines. Growing evidence suggests a link between chronic inflammation and hypertension. Therefore elucidating mechanisms that promote SLE hypertension may be of significant value not only to patients with SLE, but also for better understanding the basis for essential hypertension.