1,721,070 research outputs found
What we know about oxidative stress in patients with chronic kidney disease on dialysis-clinical effects, potential treatment, and prevention
No full textPatients with chronic kidney disease (CKD) experience accelerated atherosclerosis leading to excessive cardiovascular death. This cannot be fully explained by traditional cardiovascular risk factors. Oxidative stress is currently receiving attention as an important pathogenetic mediator of tissue damage. Oxidative stress is highly prevalent in patients with CKD. Increased prooxidant activity (age, diabetes, hypertension, inflammation, incompatibility of dialysis membranes, and solutions) goes together with reduced antioxidant defense (reduced activity of the glutathione system, low levels of vitamin E, C). Oxidative stress has been linked to several surrogate markers of atherosclerosis in patients with CKD, such as endothelial dysfunction and intima-media thickness. However, large epidemiological studies testing hard endpoints are lacking. Oxidative stress may also influence response to erythropoiesis-stimulating agents. Among possible therapeutic approaches, the use of vitamin E seems to be the most promising. Given orally, it has been shown to significantly improve cardiovascular outcomes in a relatively small clinical trial. When bonded to biocompatible dialysis membranes, it may be effective in improving erythropoiesis-stimulating agents' responsiveness. Similarly, vitamin C may be effective in reducing cardiovascular events in haemodialysis patients. Further well-designed, randomized controlled clinical trials with antioxidants are required to establish their potential to make a substantive difference in clinical practice
Mechanisms of disease : the role of aldosterone in kidney damage and clinical benefits of its blockade
No full textIn the past 10 years, many widely accepted concepts relating to aldosterone production and its pathogenetic role have changed. We now know that aldosterone is produced not only by the zona glomerulosa of the adrenal cortex, but also in the heart, blood vessels, kidney and brain; such extra-epithelial production occurs mainly during tissue repair. Also, increased aldosterone levels contribute to vessel inflammation, oxidative stress, endothelial dysfunction and organ damage. As such, aldosterone has a key role in the development of myocardial fibrosis. Anti-aldosterone treatment has proven effective in patients with heart failure. Experimental evidence regarding the role of aldosterone in kidney damage has accumulated. Aldosterone infusion can counteract the beneficial effects of treatment with angiotensin-converting-enzyme inhibitors, causing more-severe proteinuria and an increased number of vascular and glomerular lesions; treatment with aldosterone antagonists can reverse these alterations. Preliminary observations in pilot studies in humans confirm the experimental findings, supporting the hypothesis that aldosterone antagonists are renoprotective in clinical practice. Studies in larger populations with longer follow-up are needed to confirm this theory
Biosimilars and Regulatory Authorities
No full textThe patent expirations for many biotechnological medicines have prompted the development of copies of biological medicinal products. Unlike generics, biosimilars are similar but not identical to their reference product, because their chemical characteristics are directly related to the manufacturing process which cannot be precisely duplicated. The regulatory policy for biosimilars is complex and in Europe it is regulated mainly by guidelines issued by the European Medicines Agency (EMEA); additional product-class specific guidelines have been developed as in the case of recombinant human erythropoietin (rHuEPO). In 2008, the experience gained with this drug has prompted the development of a new guideline, currently in draft. In this review we critically discuss aspects related to EMEA guidelines, particularly focusing on rHuEPO.</jats:p
Il Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) modula il fenotipo di membrana di fibroblasti di gengiva umana
No full textIl Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) modula il fenotipo di membrana di fibroblasti di gengiva umana
No full text- …
