This study was registered at clinicaltrials.gov as NCT00435734. Am J Clin Nutr 2010; 91: 1165-71.”
“The Banff 2007 classification allows chronic rejection to be differentiated based on clinicopathological characteristics evidenced by two independent immunologic mechanisms; chronic active antibody-mediated selleck products rejection and chronic active T-lymphocyte mediated rejection. However, several incompletely understood issues concerning chronic active antibody-mediated rejection remain. Chronic active antibody-mediated rejection is characterized by C4d deposition in the capillary basement membrane(PTC), the presence of circulating anti-donor antibodies(DSA), and morphologic
evidence of chronic tissue injury such as glomerular double contours compatible with transplant glomerulopathy (TPG), PTC basement membrane multilayering, interstitial fibrosis/tubular atrophy, and fibrous arterial intimal thickening. PTC basement membrane multilayering correlates highly with TPG, and most of TPG have evidence of either C4d-positive staining or DSA. However, the proposed criteria do not apply to all situations of chronic active antibody-mediated rejection. C4d is not a magic marker YAP-TEAD Inhibitor 1 ic50 for antibody-mediated rejection. C4d staining is not always highly sensitive for detecting antibody-mediated rejection. Multi-institutional studies should be conducted to better
understand the clinicopathological context of chronic antibody-mediated rejection. These studies should include well-designed serial protocol biopsies with evaluation by electron microscopy, C4d staining performed on frozen sections, and assessment using sensitive DSA detection methods.”
“Introduction and objectives: The sensitivity of cardiovascular risk functions is low because many cardiovascular events occur in low- or intermediate-risk patients. The aim of the present study was to evaluate how the ankle-brachial index (ABI) reclassifies these patients.
Methods: We conducted a descriptive, Navitoclax transversal, multicenter study (28 centers) of 3171 randomly selected patients aged > 49 years. We studied demographic variables, clinical history and cardiovascular risk factors, ABI (defined
as pathologic if < 0.9) and 10-year cardiovascular risk with the Framingham-Wilson, REGICOR and SCORE equations, dividing risk into three categories: low (Framingham < 10%, REGICOR < 5% and SCORE < 2.5%, intermediate (10-19.9%, 5-9.9% and 2.5-4.9%, respectively) and high (>= 20%, >= 10% and >= 5%, respectively). Low- or intermediate-risk patients were reclassified as high-risk if they presented ABI <0.9.
Results: We compared patients with ABI < 0.9 and patients with ABI >= 0.9 and found the former were significantly older, more frequently men, had a worse history and more cardiovascular risk factors, and included more high-risk patients than when the classification used Framingham-Wilson (42.7% vs. 18.