Background: Inflammatory bowel disease ( IBD ) is characterized by a low prevalence of traditional risk factors, an increased aortic pulse‐wave velocity ( aPWV ), and an excess of cardiovascular events. We have previously hypothesized that the cardiovascular risk excess reported in these patients could be explained by chronic inflammation. Here, we tested the hypothesis that chronic inflammation is responsible for the increased aPWV previously reported in IBD patients and that anti‐TNFa (anti‐tumor necrosis factor‐alpha) therapy reduce aPWV in these patients. Methods and Results: This was a multicenter longitudinal study. We enrolled 334 patients: 82 patients with ulcerative colitis, 85 patients with Crohn disease, and 167 healthy control subjects matched for age, sex, and mean blood pressure, from 3 centers in Europe, and followed them for 4 years (range, 2.5–5.7 years). At baseline, IBD patients had higher aPWV than controls. IBD patients in remission and those treated with anti–TNFa during follow‐up experienced an aortic destiffening, whereas aPWV increased in those with active disease and those treated with salicylates ( P =0.01). Disease duration ( P =0.02) was associated with aortic stiffening as was, in patients with ulcerative colitis, high‐sensitivity C‐reactive protein during follow‐up ( P =0.02). All these results were confirmed after adjustment for major confounders. Finally, the duration of anti–TNFa therapy was not associated with the magnitude of the reduction in aPWV at the end of follow‐up ( P =0.85). Conclusions: Long‐term anti–TNFa therapy reduces aPWV , an established surrogate measure of cardiovascular risk, in patients with IBD . This suggests that effective control of inflammation may reduce cardiovascular risk in these patients.

Obesity is a well‐known risk factor for the development and progression of chronic kidney disease. Recently, para‐perirenal ultrasonographic fat thickness (PUFT) has shown to correlate with both total and visceral fat better than body mass index (BMI), waist circumference (WC), and other indices of obesity. Moreover, a local paracrine and mechanical action of the PUFT on kidney has been described in recent studies. Aim of our study was to assess the relationship between glomerular filtration rate (GFR) and PUFT in comparison with other anthropometric and ultrasonographic indices of adiposity. Two hundred and ninety‐six hypertensive patients were enrolled. PUFT, cutis‐rectis thickness and rectis‐aorta thickness were obtained by ultrasonography. Anthropometric measures of adiposity were also measured. Estimated GFR was calculated using the CKD‐EPI equation. Higher PUFT values were observed in patients with impaired renal function (P < 0.001), whereas no differences in BMI and WC were shown between groups divided by GFR. PUFT significantly correlated with GFR in all patients (r = −0.284; P < 0.001), with no differences in groups divided by sex, diabetes, or BMI. This association held in multivariate analyses also after correction for confounding factors, including other adiposity indices (P < 0.001). When receiver operating characteristic curves were built to detect a eGFR < 60 mL/minutes per 1.73 m², a PUFT value ≤3.725 cm showed a negative predictive value of 94.0%, with the largest area under the curve (AUC: 0.700) among the variables considered. In conclusion, the relationship between PUFT and GFR seems to be more accurate and less influenced by the bias affecting traditional indices of adiposity.

Recent data suggest that renal haemodynamic parameters obtained by duplex Doppler sonography, especially the intrarenal resistive index (RI), may be associated with systemic vascular changes. However, conflicting data exist about the independent relationship between aortic stiffness and RI. The aim of this study was to evaluate the relationship between RI and arterial stiffness, assessed by aortic pulse wave velocity (aPWV), in hypertensive patients. Cross-sectional study. We enrolled 264 hypertensive subjects aged between 30 and 70 years. They were divided into two groups, either with normal renal function (n = 140) or with chronic kidney disease (CKD) (n = 124). Each patient underwent assessment of ultrasonographic renal RI and measurement of aPWV through oscillometric device. Patients with renal RI>0.7 showed higher values of aPWV, both in the overall population (p < 0.001) and in the subgroups with (p < 0.01) and without CKD (p < 0.01). Moreover, statistically significant correlations were observed between aPWV and RI in the whole population (r = 0.38, p < 0.001) and in the subgroups with (r = 0.35, p < 0.001) and without CKD (r = 0.31, p < 0.001). These correlations held even after adjustment for several confounding factors in multivariate analyses. Our results seem to corroborate the concept that the RI may be considered as a marker of systemic vascular changes and therefore a predictor of cardiovascular risk.