Association of Higher Advanced Oxidation Protein Products (AOPPs) Levels in Patients with Diabetic and Hypertensive Nephropathy.

Background and Objectives: Diabetes mellitus (DM) and hypertension (HT) are characterized by cell damage caused by inflammatory and metabolic mechanisms induced by alteration in reduction-oxidative status. Serum advanced oxidation protein products (AOPP) are new markers of protein damage induced by oxidative stress. We evaluated serum levels of AOPP in a cohort of patients with DM and HT, with or without renal complications, compared with a control healthy population. Materials and Methods: The study group comprised of 62 patients with type 2 DM and 56 with HT. The 62 patients affected by DM were further distinguished in 24 subjects without renal impairment, 18 with diabetic nephropathy (DN), 20 with chronic kidney disease (CKD) stage 2-3 secondary to DN. The subgroup of 56 patients with primary HT comprised 26 subjects without renal complications and 30 with CKD (stage 2-3) secondary to HT. Thirty healthy controls, matched for age and sex, were recruited among blood donors. Results: Increased AOPP levels were found in DM patients compared with healthy subjects, although not significantly. This index was higher and more significant in patients with DN and CKD secondary to DN than in DM patients without nephropathy (p < 0.05) or controls (p < 0.0001). Patients with HT and with kidney impairment secondary to HT also had significantly higher AOPP serum levels than controls (p < 0.01 and p < 0.0001, respectively). There were no significant differences in mean AOPP levels among DM and HT patients. Conclusion: Our study showed that oxidative stress was higher in diabetic or hypertensive subjects than in healthy controls and, in particular, it appeared to be more severe in patients with renal complications. We suggest that the assessment of AOPP in diabetic and hypertensive patients may be important to predict the onset of renal failure and to open a new perspective on the adoption of antioxidant molecules to prevent CKD in those settings.

Carotid artery diameter and wall stiffness in proteinuric renal disease without severely reduced kidney function.

PURPOSE: To evaluate the carotid artery diameter, and wall thickness and stiffness in patients with glomerulopathy and proteinuria without severely reduced kidney function. METHODS: We compared 30 control subjects to 30 patients with glomerular disease, proteinuria, and glomerular filtration rate > 30 ml/min/1.73 m(2) : membranous glomerulonephritis (n = 13), minimal change disease (n = 2), focal and segmental glomerulosclerosis (n = 3), IgA nephropathy (n = 5), lupus nephritis (n = 5), antiphospholipid antibody nephropathy (n = 1), cryoglobulinemic glomerulonephritis (n = 1). The laboratory evaluations included carotid artery diameter, intima-media thickness, and stiffness measurements. RESULTS: Carotid cross-sectional area of intima-media complex was thicker in patients (18.6 ± 1.4 [x ± SEM]) than in controls (14.8 ± 0.6 mm(2) , p = 0.014), as was carotid artery wall stiffness (8.96 ± 0.86 versus 5.65 ± 0.38, [x ± SEM], p < 0.01). This difference remained significant after adjustment for age, sex, and metabolic cardiovascular risk factors: carotid stiffness was 9.19 ± 0.67 (99% confidence interval [CI] 7.40-10.98)] in patients and 4.80 ± 0.75 (99% CI 2.79-7.11) in controls; adjusted mean difference 4.40 (99% CI 1.46-7.34); p <0.001. CONCLUSIONS: This study showed, for the first time, signs of altered structural and elastic properties of the arterial wall in patients with proteinuria and glomerular disease without severely reduced kidney function.

Endothelial dysfunction in chronic renal failure.

Cardiovascular disease is a very early phenomenon in the course of chronic renal failure, and increases continuously with decrease of renal function. Endothelial dysfunction seems to be a starting point in vascular changes leading to atherosclerosis and artery calcification. Endothelium, considered the largest organ in the body, has many functions. It senses mechanical and hormonal stimuli and in response the endothelial cells secrete a range of compounds which modulate vascular tone, coagulation, cell proliferation, and inflammation. The central role of endothelium in the development of vascular disease has led to identification of new relevant biomarkers and methods to estimate endothelial function and injury. Arterial stiffness, which is not an early phenomenon in endothelial dysfunction but a common complication of chronic renal failure may be evaluated through Pulse Wave Velocity and Augmentation Index obtained by pulse-wave analysis. Aortic stiffness is an independent predictor of cardiovascular morbidity and mortality in patients with hypertension. A new fascinating aspect of research in endothelial function is rising through the studies on endothelial progenitor cells. These are primitive bone marrow cells that have the ability to mature into endothelial cells and have a physiologic role in the repair of endothelial lesions.

Air pollution and carotid arterial stiffness in children.

BACKGROUND AND PURPOSE: Many studies unequivocally indicate that air pollution is directly linked to the adverse cardiovascular outcomes in the general population. No data are currently available on cardiovascular effects of exposure to trafficked roads in healthy children. Distance of the residence to a major road has been shown to be a useful proxy for long-term traffic exposure and seem to be more consistently associated with atherosclerosis than particulate matter 2.5. The aim of this study was to investigate a possible association between the distance to a major road and carotid arterial subclinical markers of atherosclerosis in a group of children in Italy. METHODS: The participants consisted of 52 healthy children living in a small town of the Amalphitan Coast with only one highly trafficked road. All children underwent an ultrasound carotid arterial examination. RESULTS: A statistically significant difference was found in carotid arterial stiffness between children living closer to the main street and other children, both those living between 330 and 730 metres from the main street and those living more than 750 metres from the main street. No significant differences were detectable in carotid arterial thickness and arterial blood pressure among the three groups of children. CONCLUSION: This study provides evidence in support of an association of exposure to air pollution with early atherosclerotic markers in healthy children. Impaired vascular health in childhood and adolescence gives further substance to the hypothesis that traffic exhausts are relevant to cardiovascular diseases even early in life.