In subjects with type 2 diabetes and hypertension but with normoalbuminuria, the use of trandolapril plus verapamil and trandolapril alone decreased the incidence of microalbuminuria to a similar extent. The effect of verapamil alone was similar to that of placebo.

Abstract. Transplant renal artery stenosis (TRAS) is a recognized, potentially curable cause of posttransplant arterial hypertension, allograft dysfunction, and graft loss. It usually occurs 3 mo to 2 yr after transplantation, but early or later presentations are not uncommon. The prevalence ranges widely from 1 to 23% in different series, reflecting the heterogeneous criteria used to establish the diagnosis, the different manner of preservation of the graft, and surgical expertise. Reported cases are progressively increasing in parallel with the use of non-invasive investigation procedures, such as Doppler ultrasonography and magnetic resonance (MR) angiography,

It is known that changes in blood flow induce vascular remodeling and that shear stress, the tractive force acting on the vessel wall due to blood flowing, influences endothelial cell function. The aim of the present study was to investigate the relation between changes in pulsatile shear forces and arterial remodeling in response to chronic elevation in blood flow within the radial artery. The authors studied vessel diameter, flow rate, and shear stress in the radial artery of uremic patients before and after surgical creation of a native arteriovenous fistula for hemodialysis access. For this purpose, the authors used echo-color-Doppler ultrasound to perform diameter and blood velocity measurements. Time-function blood flow rate and wall shear stress were calculated based on arterial diameter, center-line velocity wave-form, and blood viscosity, using a numerical method developed according to Womersley's theory for unsteady flow in tubes. The results confirmed that the radial artery diameter increases in response to a chronic increase in blood flow in uremic patients. Moreover, it seems that the radial artery dilates in such a way as to maintain the peak wall shear stress constant, suggesting that endothelial cells sense the maximum rather than the time-averaged wall shear stress. This finding may lead to further understanding of the mechanisms responsible for endothelial response to physical stimulation by flowing blood.

At the moment, there are no effective therapies to prevent or slow the progression of autosomal dominant polycystic kidney disease (ADPKD). Radiologic evaluations are used to monitor volume of renal cysts and parenchyma during disease evolution. Volumetric quantifications based on computed tomography were used to investigate the relation between structural and functional changes in patients with advanced-stage ADPKD. By use of image-processing techniques, volume of kidneys, renal cysts, fully enhanced parenchyma, and faintly contrast-enhanced parenchyma, referred to as intermediate, was estimated. GFR measurements and computed tomography evaluations were repeated 6 mo later. No statistically significant correlations were found between volumes of cysts and parenchyma and intermediate volume and GFR. However, the ratio of intermediate over parenchymal volume strongly correlated with GFR (r ‫؍‬ ؊0.81, P < 0.001). In addition, there were significant correlations between percentage changes in intermediate volume (absolute or relative to parenchyma) and GFR changes during the observation period (r ‫؍‬ ؊0.70 and r ‫؍‬ ؊0.75, P < 0.01). These data support the hypothesis of a significant relation between radiologic appearance of renal structure and functional changes and suggest new ways that renal dysfunction in ADPKD may be predicted. Further work is necessary to determine the nature of faintly contrast-enhanced parenchyma and its role in renal functional loss.Clin J Am Soc Nephrol 1: 754 -760, 2006. doi: 10.2215/CJN.02251205 E ight to 10% of patients with ESRD are affected by autosomal dominant polycystic kidney disease (ADPKD), a hereditary disease whose progression is largely related to the development and growth of cysts and the concomitant disruption of normal renal tissue (1,2). Patients who have AD-PKD present faster decline in GFR compared with those who have other renal diseases, and current therapies are inefficient at arresting or even slowing the progressive loss of renal function. As a result, approximately 50% of patients who have ADPKD need renal replacement therapy by 60 yr of age (1).Besides monitoring renal function by standard measurements, follow-up of patients with ADPKD is based largely on radiologic investigations that are performed with ultrasounds, computerized tomography (CT), or magnetic resonance imaging, with the aim of evaluating renal cyst morphology and volume and estimating the amount of residual renal parenchyma. Investigation of the three-dimensional structures in kidneys that are affected by ADPKD usually takes place on bidimensional images that are analyzed by conventional radiologic procedures, which do not allow quantification of the real volume extension of renal cysts and parenchyma in the entire organs. Characterization of the progression of the disease in terms of kidney structural changes at the single-patient level therefore is not feasible; neither is the evaluation of the effect of therapeutic interventions that aim to interfere with the process of epithelial cell fluid se...