The primary cause of morbidity and mortality in renal transplantation is cardiovascular disease. Increased oxidative stress implies a greater degree of atherogenesis in these patients. N-acetylcysteine (NAC) which has a thiol group that is the source of l-cysteine and reduced glutathione, acts against atherosclerosis via a decrease in apoptosis, vasoconstriction, and endothelial dysfunction. Experimental models have examined the antioxidant effects of NAC during and after ischemia-reperfusion, but few studies have shown an effect in renal transplantation in human beings. In 8 months, we studied the effect of NAC treatment on oxidative stress, lipids, and renal function in 25 patients with stable renal function and no diabetes after transplantation. Data were collected on oxidative parameters: malondialdehyde, glutathione peroxidase, catalase, superoxide dismutase, glutathione reductase, lipid profile, and renal function (creatinine concentration, Cockroft-Gault formula, and Modified Diet in Renal Disease study). There were no significant differences in oxidative profile before and after treatment with NAC. The mean serum high-density lipoprotein cholesterol fraction increased after treatment and showed a significant positive correlation with glutathione peroxidase (r = 0.495). Serum creatinine concentration decreased, and Cockroft-Gault and Modified Diet in Renal Disease study estimates of renal function increased in the treatment period. In conclusion, NAC treatment in patients with stable renal function after transplantation increased high-density lipoprotein cholesterol and antioxidant molecules in relation to glutathione peroxidase, with a positive influence on renal function.
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http://dx.doi.org/10.1016/j.transproceed.2008.08.109 | DOI Listing |
Eur Heart J Acute Cardiovasc Care
January 2025
Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Background: Closing the evidence-practice gap for the treatment of acute coronary syndrome (ACS) is central to improving quality of care. Under the European Society of Cardiology (ESC) framework, we aimed to develop updated quality indicators (QIs) for the evaluation of quality of care and outcomes for patients with ACS.
Methods: A Working Group of experts including members of the ESC Clinical Practice Guidelines Task Force for ACS, Acute CardioVascular Care Association and European Association of Percutaneous Cardiovascular Interventions followed the ESC methodology for QI development.
Epigenetics
December 2025
Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA.
RNA N6-methyladenosine (m6A) plays diverse roles in RNA metabolism and its deregulation contributes to tumor initiation and progression. Clear cell renal cell carcinoma (ccRCC) is characterized by near ubiquitous loss of followed by mutations in epigenetic regulators , , and . Mutations in , a histone H3 lysine 36 trimethylase (H3K36me3), are associated with reduced survival, greater metastatic propensity, and metabolic reprogramming.
View Article and Find Full Text PDFJ Magn Reson Imaging
January 2025
Department of Radiology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Background: As ferroptosis is a key factor in renal fibrosis (RF), iron deposition monitoring may help evaluating RF. The capability of quantitative susceptibility mapping (QSM) for detecting iron deposition in RF remains uncertain.
Purpose: To investigate the potential of QSM to detect iron deposition in RF.
Curr Opin Clin Nutr Metab Care
January 2025
Institute for Applied Human Physiology, Bangor University, Bangor, UK.
Purpose Of Review: In people living with kidney disease (KD) Fatigue is a whole-body tiredness that is not related to activity or exertion. Often self-reported, fatigue is a common and highly burdensome symptom, yet poorly defined and understood. While its mechanisms are complex, many fatigue-related factors may be altered by exercise and physical activity intervention.
View Article and Find Full Text PDFJ Am Soc Nephrol
January 2025
Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Background: Deficiency of adiponectin and its downstream signaling may contribute to the pathogenesis of kidney injury in type 2 diabetes. Adiponectin activates intracellular signaling via adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2), but the role of AdipoR-mediated signaling in glomerular injury in type 2 diabetes remains unknown.
Methods: The expression of AdipoR1 in the kidneys of people with type 2 diabetes and the expression of podocyte proteins or injury markers in the kidneys of AdipoR1-knockout (AdipoR1-KO) mice and immortalized AdipoR1-deficient human podocytes were investigated by immunohistochemistry and immunoblotting.
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