Systemic lupus erythematosus (SLE) is a chronic multi-system autoimmune disease characterized by circulating autoantibodies, prevalent hypertension, renal injury, and cardiovascular disease. Onset of the disease often occurs in young women of child-bearing age. Although kidney involvement is common to patients with SLE, little is known about temporal changes in renal hemodynamic function and its relationship to the pathogenesis of hypertension during autoimmune diseases. We hypothesized that the loss of immunological tolerance and subsequent production of autoantibodies in SLE leads to impaired renal hemodynamic function that precedes the development hypertension. Female NZBWF1 (SLE) mice and female NZW/LacJ (control) mice were instrumented with carotid artery and jugular vein catheters to determine mean arterial pressure (MAP) and glomerular filtration rate (GFR) respectively at ages 15, 20, 24, 28, 31, and 34 weeks. In addition, urinary albumin excretion, blood urea nitrogen (BUN), circulating autoantibodies, and glomerulosclerosis were assessed at each age. Levels of circulating autoantibodies are increased between 24 and 28 weeks of age in NZBWF1 mice, whereas autoantibodies are unchanged in control mice. GFR is significantly increased at 28 weeks of age in NZBWF1 mice followed by a sharp decline at 34 weeks of age. NZBWF1 mice have an increase in MAP that occurs by 34 weeks of age. These data show that changes in circulating autoantibodies, renal hemodynamic function, and glomerular injury occur in NZBWF1 mice prior to changes in MAP, suggesting an important mechanistic role for autoimmunity to directly impair renal hemodynamic function and promote the development of hypertension.