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Background and Aims: A high prevalence of atherosclerotic lesions characterizes patients with chronic kidney disease, though there is little data on the relationship between kidney function and atherosclerotic changes in the healthy population or in people with no known renal impairment. The aim of our study was to analyze, in a comprehensive general population with no known kidney disease, the relationship between renal function and subclinical carotid atherosclerotic damage.Methods and Results: A general real-life population of 611 participants (233 males and 378 females; age ≥18 years) with no known kidney failure was selected for the study. The glomerular filtration rate (GFR) was estimated according to the CKD-EPI equation. Carotid intima-media thickness (c-IMT) and plaques were assessed by duplex Doppler ultrasonography of the carotid vessels. The main laboratory and metabolic parameters were evaluated in all participants. When we divided the overall study population into tertiles according to GFR values (I tertile <85; II tertile: 85-99; III tertile >99 ml/min/1.73 m2), the c-IMT mean values and the prevalence of carotid plaques decreased with the increasing tertile of GFR. On univariate analysis, c-IMT was significantly correlated with eGFR (r = -0.33; p < 0.001), serum creatinine (r = 0.17; p < 0.001), and other variables such as age, systolic blood pressure, waist circumference, fasting or random glycemia, and glycated hemoglobin (HbA1c). On multiple regression analysis, serum creatinine was associated with c-IMT (β = 0.069; p = 0.017), independent of other covariates.Conclusion: Our study seems to suggest the importance of early identification of people with near normal or mildly decreased renal function due to its association with carotid atherosclerosis. [ABSTRACT FROM AUTHOR]

Abstract: Background and Aims: Metabolic syndrome (MS) has been mainly related to insulin resistance, but the role of changes in insulin secretion has not been thoroughly investigated. Methods and Results: Using an oral glucose tolerance test (OGTT) we studied beta-cell function and insulin sensitivity in subjects with normal fasting glucose with and without MS, and their relationship to fatty liver which was evaluated by abdominal-ultrasonography. In MS early phase insulin secretion, as measured by insulinogenic index (IG30), was increased (p <0.05) independently from insulin sensitivity. Furthermore IG30 was progressively higher as the number of factors needed for the diagnosis of MS increased (p <0.01). Insulin and C-peptide AUC were also increased (p <0.01 and p <0.05, respectively) but, in contrast to IG30, these differences disappeared when ISI was used as a covariate. After OGTT, 51% of the subjects with MS had altered post-load glucose tolerance compared to 24.9% without MS (p <0.01). In both groups, the altered glucose tolerance was associated with a similar IG30 reduction. In normo-tolerant subjects with MS the IG30 was higher (+54.1%, p <0.01), and this elevation occurred irrespective of ISI; however, the beta-cell compensatory capacity for insulin resistance (disposition index) was impaired (p <0.001). Fatty liver was more frequent (p <0.001) and more severe (p <0.01) in MS, and it was significantly related to total AUC-insulin (p <0.001), independently from ISI. Conclusion: These findings indicate that the prevalence of altered tolerance is more frequent in subjects with normal fasting glucose and MS. The hyperinsulinemia might not only be an adaptive response to insulin resistance, but a primary defect of beta-cell function contributing to glucose intolerance. [Copyright &y& Elsevier]

BACKGROUND: A supplemented very-low-protein diet (sVLPD) seems to be safe when postponing dialysis therapy. STUDY DESIGN: Prospective multicenter randomized controlled study designed to assess the noninferiority of diet versus dialysis in 1-year mortality assessed by using intention-to-treat and per-protocol analysis. SETTING & PARTICIPANTS: Italian uremic patients without diabetes older than 70 years with glomerular filtration rate of 5 to 7 mL/min (0.08 to 0.12 mL/s). INTERVENTION: Randomization to an sVLPD (diet group) or dialysis. The sVLPD is a vegan diet (35 kcal; proteins, 0.3 g/kg body weight daily) supplemented with keto-analogues, amino acids, and vitamins. Patients following an sVLPD started dialysis therapy in the case of malnutrition, intractable fluid overload, hyperkalemia, or appearance of uremic symptoms. OUTCOMES & MEASUREMENTS: Mortality, hospitalization, and metabolic markers. RESULTS: 56 patients were randomly assigned to each group, median follow-up was 26.5 months (interquartile range, 40), and patients in the diet group spent a median of 10.7 months (interquartile range, 11) following an sVLPD. Forty patients in the diet group started dialysis treatment because of either fluid overload or hyperkalemia. There were 31 deaths (55%) in the dialysis group and 28 deaths (50%) in the diet group. One-year observed survival rates at intention to treat were 83.7% (95% confidence interval [CI], 74.5 to 94.0) in the dialysis group versus 87.3% (95% CI, 78.9 to 96.5) in the diet group (log-rank test for noninferiority, P < 0.001; for superiority, P = 0.6): the difference in survival was -3.6% (95% CI, -17 to +10; P = 0.002). The hazard ratio for hospitalization was 1.50 for the dialysis group (95% CI, 1.11 to 2.01; P < 0.01). LIMITATIONS: The unblinded nature of the study, exclusion of patients with diabetes, and incomplete enrollment. CONCLUSION: An sVLPD was effective and safe when postponing dialysis treatment in elderly patients without diabetes.Copyright © 2007 by National Kidney Foundation, Inc. [ABSTRACT FROM AUTHOR]

Abstract: Background: Few studies examined the risk factors of asymptomatic bacteriuria, showing contradictory results. Our study aimed to examine the association between different clinical and laboratory parameters and asymptomatic bacteriuria in internal medicine patients. Materials and methods: 330 consecutive hospitalized subjects, asymptomatic for urinary tract infections (UTIs), underwent to microscopic examination of urine specimens. 100 subjects were positive for microscopic bacteriuria and were recruited into the study. At the quantitative urine culture 31 subjects of study population were positive while 69 subjects were negative for bacteriuria. Results: The analysis of clinical characteristics showed that the two groups of subjects (positive and negative urine culture for bacteriuria) were significant different (p<0.05) about obesity (76.7% vs 42% respectively), metabolic syndrome (80.6% vs 44,9%), cholelithiasis (35.5% vs 13,2%) and iron deficiency anemia (80.6% vs 53,6%). The univariate analysis showed that only obesity, cholelithiasis and iron deficiency anemia were positively associated with positive urine culture for bacteriuria (Odds Ratios [OR]=3.79, p=0.0003; OR=2,65, p=0.0091; OR=2.63, p=0.0097; respectively). However, the multivariate analysis by logistic regression showed that only obesity and iron deficiency anemia, independently associated with positive urine culture for bacteriuria (OR=3.9695, p=0.0075; OR=3.1569, p=0.03420 respectively). Conclusions: This study shows that obesity and iron deficiency anemia are independent risk factors for asymptomatic bacteriuria. [Copyright &y& Elsevier]

Abstract: Aims: Occlusive coronary artery disease (CAD) is associated with left ventricular (LV) remodeling, LV systolic dysfunction, and heart failure. The BEAUTIFUL Echo substudy aimed to evaluate the effects of heart rate reduction with ivabradine on LV size (primary end-point: change in LV end-systolic volume index [LVESVI]) and function and the cardiac biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP). Methods and results: The substudy was carried out in 86 centers participating in the BEAUTIFUL study. 2D echocardiography was performed at baseline, and after 3 and 12months in patients with stable CAD and LV systolic dysfunction receiving ivabradine or placebo at the same time-points. All data were read and analyzed centrally. Of 525 patients completing the study, 426 had adequate echocardiographic readings (n =220 ivabradine; n =206 placebo). Treatment with ivabradine was associated with a decrease in the primary end-point LVESVI (change from baseline to last value, −1.48±13.00mL/m2) versus an increase with placebo (1.85±10.54mL/m2) (P =0.018). There was an increase in LV ejection fraction with ivabradine (2.00±7.02%) versus no change with placebo (0.01±6.20%) (P =0.009). Reduction in LVESVI was related to the degree of heart rate reduction with ivabradine. There were no differences in any other echocardiographic parameters or NT-proBNP. Change in LVESVI was related to the log change in NT-proBNP in the ivabradine group only (r =0.18, P =0.006). Conclusions: Our observations suggest that ivabradine may reverse detrimental LV remodeling in patients with CAD and LV systolic dysfunction. [ABSTRACT FROM AUTHOR]

Objectives: This study was designed to investigate whether poor responders to thienopyridines after clopidogrel remain so even after ticlopidine administration (class effect) or whether a drug-specific effect exists between currently available thienopyridines. Background: Whether clopidogrel poor responders also display inadequate platelet inhibition after ticlopidine administration remains undefined. Methods: Platelet aggregation (PA) was measured in 143 patients, while they were taking aspirin, with light transmission aggregometry using adenosine diphosphate as an agonist at baseline (T0) and at clopidogrel steady state (T1). After T1) clopidogrel was stopped and substituted with ticlopidine. Then PA was assessed at ticlopidine steady state (T2). Resistance was defined as an absolute difference between T0 and after-treatment (T1 or T2) PA < or =10%. Results: Clopidogrel and ticlopidine responsiveness was normally distributed; PA at T1 did not differ compared with T2. Thirty (21%) and 28 (19%) patients were clopidogrel and ticlopidine nonresponders, respectively. Only 5 patients (3.5%) were nonresponders to both clopidogrel and ticlopidine (class effect), whereas 25 patients (83%) who were clopidogrel nonresponders at T1 were responsive to ticlopidine, reaching a higher level of platelet inhibition at T2 (PA 69 +/- 15 vs. 44 +/- 18, p < 0.01) (drug-specific response). On the other hand, 23 patients who were responsive to clopidogrel showed resistance to ticlopidine at T2 (PA 46 +/- 15 vs. 70 +/- 15, p < 0.01) (drug-specific response). Conclusions: Poor responsiveness to either clopidogrel or ticlopidine at steady state was common, whereas nonresponders to both drugs were relatively infrequent (3.5%, 95% confidence interval 1.5% to 7.9%), suggesting that poor response to thienopyridines may frequently be a drug-specific mechanism. [ABSTRACT FROM AUTHOR]