The internist and the renal resistive index: truths and doubts.

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.

Adherence to antihypertensive therapy affects Ambulatory Arterial Stiffness Index.

BACKGROUND: A major contributor to poor blood pressure (BP) control is nonadherence to therapy, which remains poorly recognized by physicians. The prevention of hypertension-induced changes in arterial wall, namely increased arterial stiffness and peripheral vascular resistance, is a reasoned adequate end-point of hypertension treatment. Indirect measurement of these arterial factors can be derived from the analysis of 24-hour Ambulatory BP Monitoring (24 h-ABPM). This pilot study evaluated the association between antihypertensive therapy adherence and 24 h-ABPM-derived parameters in hypertensive patients. METHODS: We studied 42 hypertensive patients (70±10 years) in chronic antihypertensive therapy. Patients were divided according to the Morisky Medication Adherence Scale (MMAS) in Low-Adher (MMAS <6) and High-Adher (MMAS 6-8) groups. The Ambulatory Arterial Stiffness Index (AASI) and its symmetric calculation (Sym_AASI) were derived from 24 h-ABPM. A bivariate logistic regression analysis was performed to evaluate the predictive value of MMAS for increased AASIs (i.e. above the median). RESULTS: Low-Adher group (n=17) showed higher AASIs compared to High-Adher group (n=25). The two groups were similar in terms of BP burden at the 24 h-ABPM. AASIs were inversely related to MMAS. MMAS resulted a predictor for both increased AASI (O.R. 0.49, 95% CI 0.31-0.76, P<0.01) and increased Sym_AASI (O.R. 0.67, 95% CI 0.47-0.95, P=0.026). After adjustment for PP, age and nocturnal diastolic BP reduction, MMAS persisted as an inverse predictor only of increased AASI. MMAS was also related to the diastolic vs systolic BP correlation coefficient r. CONCLUSIONS: Low adherence to antihypertensive therapy seems to be associated with increased standard AASI. In this setting, AASI could represent an additional information derived from the 24 h-ABPM in hypertensive patient evaluation.