Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
-
The term uraemic myopathy has been used loosely to describe the skeletal muscle abnormalities in uraemic patients. However, it does not fully explain the observed abnormalities as recent research has documented a normal skeletal muscle physiology in the presence of reduced muscle force, selective structural changes and significant muscle wasting. Ageing is associated with sarcopenia (muscle wasting) and an increase in the prevalence of chronic kidney disease (CKD), which accelerates the normal physiological muscle wasting. ⋯ Uraemic sarcopenia presents a high probability for morbidity and mortality and consequently a high priority for muscle wasting prevention and treatment in these patients. Perhaps, the use of the term 'uraemic sarcopenia' would provide recognition by the renal community for this devastating problem. The purpose of this review is to relate the findings of the recent publications that describe abnormalities in uraemic skeletal muscle to the possible pathogenesis of muscle wasting and its consequences in patients with CKD.
-
Nephrol. Dial. Transplant. · Jul 2014
Editorial ReviewA basic science view of acute kidney injury biomarkers.
Over the last decade, significant progress has been made in the identification and validation of novel biomarkers as well as refinements in the use of serum creatinine as a marker of kidney function. These advances have taken advantage of laboratory investigations, which have identified these novel molecules that serve important biological functions in the pathogenesis of acute kidney injury (AKI). As we advance and validate these markers for clinical studies in AKI, we recognize that they serve not only to improve our understanding of AKI, but they could also serve as potential targets for the treatment of AKI. This review will underscore the biological basis of specific biomarkers that will contribute to the advancement in the treatment and outcomes of AKI.
-
Nephrol. Dial. Transplant. · May 2014
ReviewNovel insights from genetic and epigenetic studies in understanding the complex uraemic phenotype.
Like in many other common complex disorders, studies of chronic kidney disease (CKD) can now make use of the increasing knowledge of the human genome, its variations and impact on disease susceptibility, initiation, progression and complications. Such studies are facilitated by novel readily available high through-put genotyping methods and sophisticated analytical approaches to scan the genome for DNA variations and epigenetic modifications. Here, we review some of the recent discoveries that have emerged from these studies and expanded our knowledge of genetic risk loci and epigenetic markers in CKD pathophysiology. Obstacles and practical issues in this field are discussed.
-
The coagulation system has gained much interest again as new anticoagulatory substances have been introduced into clinical practice. Especially patients with renal failure are likely candidates for such a therapy as they often experience significant comorbidity including cardiovascular diseases that require anticoagulation. Patients with renal failure on new anticoagulants have experienced excessive bleeding which can be related to a changed pharmacokinetic profile of the compounds. ⋯ Recent work provides evidence that new factors such as microparticles (MPs) can influence the coagulation system in patients with renal insufficiency through their potent procoagulatory effects. Interestingly, MPs may also contain microRNAs thus inhibiting the function of platelets, resulting in bleeding episodes. This review comprises the findings on the complex pathophysiology of coagulation disorders including new factors such as MPs and microRNAs in patients with renal insufficiency.