A significant link has been shown between aortic stiffening and renal microvascular damage, but the underlying mechanism is not fully understood. We hypothesized that alterations in central and renal hemodynamics are responsible for this link. In 133 patients with hypertension, pressure waveforms were recorded on the radial, carotid, femoral and dorsalis pedis arteries with applanation tonometry to estimate the aortic pressures and aortic (carotid-femoral) and peripheral (carotid-radial and femoral-dorsalis pedis) pulse wave velocities (PWVs). Flow-velocity waveforms were recorded on the renal segmental arteries with duplex ultrasound to calculate the resistive index (RI) as [1 – (end-diastolic velocity/peak systolic velocity)], and on the femoral arteries to calculate the reverse/forward flow index and diastolic/systolic forward-flow ratio. (Micro)albuminuria was defined as urinary albumin/creatinine ratio (UACR) ≥30mg/gCr. The renal RI (mean, 0.65±0.07) was strongly correlated (P<0.001) with the aortic pulse pressure (r=0.62), incident pressure wave (r=0.55), augmented pressure (r=0.52) and aortic PWV (r=0.51), though not with the mean arterial pressure or peripheral PWVs. The correlations remained highly significant after adjustment for confounders including age, sex, hypercholesterolemia, diabetes and serum creatinine. The renal RI was inversely correlated with the femoral reverse and diastolic forward flow indices. Both aortic pulse pressure and renal RI correlated with UACR independently of the confounders. Each 0.1 increase in renal RI was associated with a 4.6-fold increase in the adjusted relative risk of (micro)albuminuria. In conclusion, increased aortic pulse pressure due to aortic stiffening causes renal microvascular damage through altered renal hemodynamics resulting from increased peripheral resistance and/or increased flow pulsation.