Objective: Non-vitamin K oral anticoagulants (NOACs) require dose adjustment for renal function. We sought to investigate change in renal function over time in patients with atrial fibrillation (AF) and whether those on NOACs have appropriate dose adjustments according to its decline.
Methods: We included patients with AF enrolled in the Outcomes Registry for Better Informed Treatment of Atrial Fibrillation II registry treated with oral anticoagulation. Worsening renal function (WRF) was defined as a decrease of >20% in creatinine clearance (CrCl) from baseline. The US Food and Drug Administration (FDA)-approved package inserts were used to define the reduction criteria of NOACs dosing.
Results: Among 6682 patients with AF from 220 sites (median age (25th, 75th): 72.0 years (65.0, 79.0); 57.1% male; median CrCl at baseline: 80.1 mL/min (57.4, 108.5)), 1543 patients (23.1%) experienced WRF with mean decline in CrCl during 2 year follow-up of -6.63 mL/min for NOACs and -6.16 mL/min for warfarin. Among 4120 patients on NOACs, 154 (3.7%) patients had a CrCl decline sufficient to warrant FDA-recommended dose reductions. Of these, NOACs dosing was appropriately reduced in only 31 (20.1%) patients. Compared with patients with appropriately reduced NOACs, those without were more likely to experience bleeding complications (major bleeding: 1.7% vs 0%; bleeding hospitalisation: 2.6% vs 0%) at 1 year.
Conclusions: In the US practice, about one-fourth of patients with AF had >20% decline in CrCl over time during 2 year follow-up. As a result, about 3.7% of those treated with NOACs met guideline criteria for dose reduction, but of these, only 20.1% actually had a reduction.
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http://dx.doi.org/10.1136/heartjnl-2019-315792 | DOI Listing |
Background: Maintenance hemodialysis (MHD) is an effective treatment for patients with end-stage renal disease. Although MHD can prolong the survival of patients, their quality of life is lower and the fatality rate is higher. This work analyzed the factors related to the autogenous arteriovenous fistula (AVF)-like expansion of non-diabetic MHD patients by vascular ultrasound (VUS).
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First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sunitinib is a first-line targeted therapy for patients with renal cell carcinoma (RCC), but resistance represents a significant obstacle to the treatment of advanced and metastatic RCC. Metabolic reprogramming is a characteristic of RCC, and changes in metabolic processes might contribute to resistance to sunitinib. Here, we identified MTHFD2, a mitochondrial enzyme involved in one-carbon metabolism, as a critical mediator of sunitinib resistance in RCC.
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Department of Biomedical sciences, Oklahoma State University Centre for Health and Science, Oklahoma, USA.
The effect of the aqueous extract of (AAI) on gentamicin (GEN)-induced kidney injury was investigated. The study involves 20 adult male Wistar rats (housed in four separate plastic cages) such that graded dosages of AAI were administered to the experimental group for 14 days per oral (PO) before exposure to GEN toxicity (100 mg/kg) for 1 week. At the end of the study, comparisons of some markers of renal functions, antioxidant status, and inflammatory and apoptotic markers were made between the control, GEN, and AAI-pretreated groups at < .
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Copenhagen Research Center for Autoimmune Connective Tissue Diseases (COPEACT), Copenhagen University Hospital, Rigshospitalet, Denmark.
To investigate if progression of coronary artery calcification (CAC) in patients with systemic lupus erythematosus (SLE) is associated with renal and traditional cardiovascular risk factors as well as incidence of myocardial infarctions. CAC progression was evaluated by cardiac computed tomography (CT) at baseline and after 5 years. Multivariable Poisson regression was applied to investigate associations between CAC progression and baseline values for traditional cardiovascular risk factors, CAC, SLE disease duration, lupus nephritis, and renal function.
View Article and Find Full Text PDFArch Dermatol Res
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Department of Dermatology, University of Nebraska Medical Center, Omaha, NE, USA.
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