E arly abnormalities in renal haemodynamics, namely an increased afferent arteriolar resistance, have been traditionally regarded as a marker of more severe hypertension status and subclinical target organ damage. Although a large body of evidence has been accumulated over the years on this topic in the experimental animal setting, data in humans have been more difficult to be collected because of the relatively cumbersome and invasive techniques used to assess renal haemodynamics in clinical studies. More recently, the possibility to obtain functional and structural information on the renal vasculature by means of noninvasive ultrasonographic Doppler assessment has spurred a growing interest in this area. In particular, blood flow abnormalities detected by analysis of intraparenchymal arterial Doppler waveform, that is the socalled renal resistive index (RRI), have been associated with the occurrence of cardiovascular and renal events [1,2].The RRI can easily be calculated by the ratio of the difference between maximum and minimum (enddiastolic) flow velocity to maximum flow velocity: RRI ¼ (maximum velocity À minimum velocity)/maximum velocity and may theoretically range from 0 to 1. Three to five reproducible waveforms have to be obtained at interlobar or arcuate arteries in three different renal sites, and RRI values from these waveforms are averaged to compute the mean RRI for each kidney [1,2]. In healthy patients, RRI have been shown to vary from 0.58 AE 0.05 (mean AE SD) to 0.64 AE 0.04, and a value lower than 0.7 has been traditionally taken to indicate normal impedance to renal blood flow, although a considerable heterogeneity has been reported [3].As a matter of fact, the physiological mechanisms and clinical determinants of RRI are yet to be fully elucidated.Although RRI was initially proposed as an indicator of renal vascular resistance to blood flow, more recent studies suggest that vascular compliance plays a key role in shaping its values [1,2]. Using an electrical model simulating changes in vascular resistance, inductance, and compliance, a recent study helped us to clarify that intrarenal impedance to blood flow, and the RRI vary in response to changes in distal resistance with the same directionality. In contrast, impedance changed in the opposite direction to the RRI when the distal compliance, proximal compliance, or proximal resistance was modified. The stiffening of systemic vasculature triggers an increase in pulse pressure which, in turn, may lead to high RRI values. Additionally, heart rate can affect RRI because of changes in diastolic duration that affect end-diastolic velocity [2].Besides vascular and haemodynamic factors, other variables such as ureteral obstruction and interstitial renal parenchymal damage may lead to an increase in RRI. As a matter of fact, clinical-pathological correlation studies in patients with chronic kidney disease and renal transplants have reported somewhat contrasting results [1,2]. Arteriolosclerosis and tubulo-interstitial nephropathies seem to be corre...