Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
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Nephrol. Dial. Transplant. · Nov 2013
ReviewObesity and nephrology: results of a knowledge and practice pattern survey.
Obesity, the largest epidemic of modern time, carries a markedly increased risk of type-2 diabetes, cancer, fatty liver, sleep apnea, hypertension, dyslipidemia and atherosclerotic cardiovascular disease. In addition, obesity increases the risk of chronic kidney disease (CKD) and its progression to end-stage renal disease (ESRD). There are limited data regarding the basic knowledge of nephrologists on how to assess and manage obesity in the setting of CKD. ⋯ The level of understanding of the intricacies of obesity in the setting of CKD needs improvement among nephrologists. Similarly, there is no consensus regarding weight management strategies in CKD patients with obesity. Studies are needed in this orphan area of renal research.
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Nephrol. Dial. Transplant. · Nov 2013
Review Meta AnalysisAnticoagulant therapies for the prevention of intravascular catheters malfunction in patients undergoing haemodialysis: systematic review and meta-analysis of randomized, controlled trials.
Catheter malfunction (CM), including thrombosis, is associated with reduced dialysis adequacy, as well as an increased risk of catheter-related bacteraemia (CRB) and mortality. The role of alternative anticoagulant regimens for CM prevention remains uncertain. ⋯ There is uncertainty on the benefits and harms of anticoagulant therapies over conventional care for prevention of CM. Further high-quality randomized trials, including safety outcomes, are needed.
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Nephrol. Dial. Transplant. · Sep 2013
ReviewFibroblast growth factor-23: what we know, what we don't know, and what we need to know.
Traditional risk factors of cardiovascular morbidity and mortality such as hypertension, hypercholesterolemia and obesity are paradoxically associated with better outcomes in dialysis patients, and the few trials of interventions targeting modifiable traditional risk factors have yielded disappointing results in this patient population. Non-traditional risk factors such as inflammation, anemia and abnormalities in bone and mineral metabolism have been proposed as potential explanations for the excess mortality seen in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD), but without clear understanding of what the most important pathophysiologic mechanisms of these risk factors are, which ones might be ideal treatment targets and which therapeutic interventions may be effective and safe in targeting them. Among the novel risk factors, fibroblast growth factor-23 (FGF23) has recently emerged as one of the most powerful predictors of adverse outcomes in patients with CKD and ESRD. ⋯ While it is possible that 'off target' effects of FGF23 present in very high concentrations could induce LVH, this possibility is controversial, since α-klotho is not expressed in the myocardium. Another possibility is that FGF23's effect on the heart is mediated indirectly, via 'on target' activation of other humoral pathways. We will review the physiology and pathophysiology of FGF23, the outcomes associated with elevated FGF23 levels, and describe putative mechanisms of action responsible for its negative effects and potential therapeutic strategies to treat these.
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Nephrol. Dial. Transplant. · Aug 2013
Review'Biologic memory' in response to acute kidney injury: cytoresistance, toll-like receptor hyper-responsiveness and the onset of progressive renal disease.
Following the induction of ischemic or toxin-mediated acute kidney injury (AKI), cellular adaptations occur that 're-program' how the kidney responds to future superimposed insults. This re-programming is not simply a short-lived phenomenon; rather it can persist for many weeks, implying that a state of 'biologic memory' has emerged. These changes can be both adaptive and maladaptive in nature and they can co-exist in time. ⋯ However, injury-induced, and stable, epigenetic remodeling at pro-inflammatory/pro-fibrotic genes seems likely to be involved. The goal of this editorial is to highlight that the so-called 'maintenance phase' of acute renal failure is not a static one, somewhere between injury induction and the onset of repair. Rather, this period is one in which the induction of 'biologic memory' can ultimately impact renal functional recovery, extra-renal injury and the possible transition of AKI into chronic, progressive renal disease.
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Nephrol. Dial. Transplant. · Jun 2013
ReviewContrast-induced acute kidney injury: how much contrast is safe?
Iodinated contrast media (CM) are used in many investigations that a patient may undergo during the course of an in-patient stay. For the vast majority of patients, exposure to CM has no sequelae; however, in a small percentage, it can result in a worsening in renal function termed contrast-induced acute kidney injury (CI-AKI). CI-AKI is one of the leading causes of in-hospital renal dysfunction. ⋯ Unfortunately, the results of extensive research into pharmacological inventions to prevent CI-AKI remain disappointing. In this article, we briefly outline the pathophysiological mechanisms by which iodinated CM may cause CI-AKI and discuss the evidence for reducing CI-AKI by limiting contrast volumes. In particular, we review the data surrounding the use of contrast volume to glomerular filtration rate ratios, which can be used by clinicians to effectively lower the incidence of CI-AKI in their patients.