OBJECTIVE—To investigate the role of intrarenal vascular disease in the pathogenesis of nonalbuminuric renal insufficiency in type 2 diabetes. RESEARCH DESIGN AND METHODS—We studied 325 unselected clinic patients who had sufficient clinical and biochemical information to calculate an estimated glomerular filtration rate (eGFR) using the Modified Diet in Renal Disease six-variable formula, at least two estimations of urinary albumin excretion rates (AER), and a renal duplex scan to estimate the resistance index of the interlobar renal arteries. The resistance index, measured as part of a complications surveillance program, was compared in patients with an eGFR < or ≥60 ml/min per 1.73 m2 who were further stratified into normo- (AER <20), micro- (20–200), or macroalbuminuria (> 200 μg/min) categories. RESULTS—Patients with an eGFR <60 ml/min per 1.73 m2 had a higher resistance index of the renal interlobar arteries compared with patients with an eGFR ≥60 ml/min per 1.73 m2. However, the resistance index was elevated to a similar extent in patients with an eGFR <60 ml/min per 1.73 m2 regardless of albuminuric status (normo- 0.74 ± 0.01, micro- 0.73 ± 0.01, and macroalbuminuria resistance index 0.75 ± 0.11). Multiple regression analysis revealed that increased age (P < 0.0001), elevated BMI (P = 0.0001), decreased eGFR (P < 0.01), and decreased diastolic blood pressure (P < 0.01), but not an increased AER, were independently associated with an elevated resistance index in patients with impaired renal function. CONCLUSIONS—Subjects with type 2 diabetes and reduced glomerular filtration rate had similar degrees of intrarenal vascular disease, as measured by the intrarenal arterial resistance index, regardless of their AER status. The pathological mechanisms that determine the relationship between impaired renal function and AER status in subjects with type 2 diabetes remain to be elucidated.