Renal Ultrasound (and Doppler Sonography) in Hypertension: An Update

Ultrasound (US) allows the non-invasive evaluation of morphological changes of kidney structure (by means of B-Mode) and patterns of renal and extrarenal vascularization (by means of color-Doppler and contrast-enhanced US). In hypertensive subjects it offers a relevant contribution to the diagnosis of early renal damage, acute or chronic nephropathies and nephrovascular disease. However, morphological changes are often detected late and non-specific and in recent years evidence has increased regarding the clinical relevance of renal resistive index (RRI) for the study of vascular and renal parenchymal renal abnormalities. RRI is measured by Doppler sonography in an intrarenal artery, as the difference between the peak systolic and end-diastolic blood velocities divided by the peak systolic velocity. At first RRI was proved to be a marker of renal disease onset and progression; later the influence of systemic vascular properties on RRI was shown and authors claimed its use as an independent predictor of cardiovascular risk rather than of renal damage. Indeed, renal vascular resistance is only one of several renal (vascular compliance, interstitial and venous pressure), and extrarenal (heart rate, pulse pressure) determinants that concur to determine RRI individual values but not the most important one. The clinical relevance of RRI measurement as a surrogate endpoint of specific renal damage or/and as surrogate endpoint of atherosclerotic diffuse vascular damage is still debated. To summarize, from the literature: (a) In hypertensives with normal renal function and no albuminuria, especially in younger people, RRI is an early marker of renal damage that is especially useful when hypertension and diabetes concur in the same subjects. In these subjects RRI could improve current clinical scores used to stratify early renal damage. In older subjects RRI increases in accordance with the increase in systemic vascular stiffness and, because of this close relationship, RRI is also a marker of systemic atherosclerotic burden and the role of renal determinants can weaken. The clinical relevance was not specifically investigated. (b) In transplant kidney and in chronic renal disease high (>0.80) RRI values can independently predict renal failure. The recent claim that systemic (pulse pressure) rather than renal hemodynamic determinants sustain this predictive role of RRI, does not significantly reduce this predictive role of RRI. (c) Doppler ultrasound allows diagnosis and grading of renal stenosis in both fibromuscolar dysplastic and atherosclerotic diseases. Moreover, by RRI assay Doppler ultrasound can indirectly measure the hemodynamic impact of renal artery stenosis on the homolateral kidney, by virtue of the stenosis-related decrease in pulse pressure. However, in elderly subjects with atherosclerotic renal artery stenosis coexisting renal diseases can independently increase RRI by the augmentation in renal vascular stiffness and tubulo-interstitial pressure and hidden changes due to renal artery stenosis.