The renal resistive index (RRI) is measured by Doppler sonography in an intrarenal artery, and is the difference between the peak systolic and end-diastolic blood velocities divided by the peak systolic velocity. The RRI is used for the study of vascular and renal parenchymal renal abnormalities, but growing evidence indicates that it is also a dynamic marker of systemic vascular properties. Renal vascular resistance is only one of several renal (vascular compliance, interstitial and venous pressure), and extrarenal (heart rate, aortic stiffness, pulse pressure) determinants that combine to determine the RRI values, and not the most important one. RRI cannot always be considered a specific marker of renal disease. To summarize from the literature: (1) hydronephrosis, abdominal hypertension, renal vein thrombosis and acute kidney injury are all associated with an acute increase in interstitial and venous pressure that determine RRI values. In all these conditions, RRI is a reliable marker of the severity of renal damage. (2) The hemodynamic impact of renal artery stenosis can be assayed by the RRI decrease in the homolateral kidney by virtue of decreasing pulse pressure. However, renal diseases that often coexist, increase renal vascular stiffness and hide the hemodynamic effect of renal stenosis. (3) In transplant kidney and in chronic renal disease, high RRI values (>0.80) can independently predict renal and clinical outcomes, but systemic (pulse pressure) rather than renal hemodynamic determinants sustain the predictive role of RRI. (4) Higher RRI detects target renal organ damage in hypertension and diabetes when renal function is still preserved, as a marker of systemic atherosclerotic burden. Is this the fact? We attempt to answer.

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In essential hypertension, increased renal resistive index (RRI) is associated to a reduction of renal function and microalbuminuria, and to renal tubulo-interstitial damage. A tubulo-interstitial inflammatory infiltration was found in experimental models of hypertension, and serum high-sensitive C-reactive protein (hsCRP) levels correlated with urinary markers of tubulointerstitial damage in humans. We studied the relationship between RRI and serum hsCRP in hypertensives with preserved renal function, without microalbuminuria. We investigated hypertensive patients without diabetes, renal failure, microalbuminuria or major inflammatory disease. Serum levels of hsCRP were assayed. RRI was calculated by intrarenal Doppler ultrasound and considered pathologic when X0.70 or 495% of upper confidence limit expected for age decade. The renal volume-to-resistive index ratio (RV/RRI) was also calculated. We evaluated 85 patients (57 ± 14 years, 61 males). Patients with pathologic RRI (n ¼ 21) were older and had significantly higher hsCRP levels (4.70 ± 2.30 vs 2.93 ± 2.09 mg l À1 , Po0.01) compared with patients with normal RRI, as well as patients with decreased RV/RRI (n ¼ 43). HsCRP was directly related with RRI (r ¼ 0.41, Po0.001) and inversely with RV/RRI (r ¼ À0.35, Po0.001). HsCRP proved to be a significant predictor of both pathologic RRI and decreased RV/RRI, even after adjustment. In essential hypertension low-grade inflammation is associated with tubulo-interstitial damage evaluated by Doppler ultrasonography.

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