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A new study by Lo et al. presents a novel immunosuppressive combination in a clinically relevant primate model of renal allografting. Using belatacept, a fusion protein that inhibits CD28–CD80/CD86 co-stimulation, plus the mammalian target of rapamycin inhibitor sirolimus, they were able to achieve rejection-free allograft survival without the induction of memory T cells or alloantibody.
New data from Ahmed et al. show that discharge prescriptions for renin–angiotensin–aldosterone inhibitor therapy are associated with a significant reduction in all-cause mortality in elderly patients with diastolic heart failure and chronic kidney disease (CKD). These observational data support the case for prospective studies of RAAS blockade in patients with CKD and diastolic heart failure.
Recently published data from four phase 3 safety and efficacy trials show that the synthetic peptide-based, erythropoietin mimetic, peginesatide, is noninferior to conventional erythropoiesis-stimulating agents in increasing haemoglobin levels in patients with chronic kidney disease (CKD). However, peginesatide therapy increased the risk of a combined cardiovascular end point in patients with CKD not on dialysis.
Pickering et al. report that unchanging plasma creatinine levels after resuscitated cardiac arrest can indicate substantial acute kidney injury (AKI) as confirmed by increased levels of AKI biomarkers and increased mortality. This finding illustrates the limitations of plasma-creatinine-based diagnosis of AKI in early critical illness.
The Lancet publication of the Global Burden of Disease Study 2010 heralds an important milestone in our understanding of population health and disease this century. The articles highlight the value of this collaboration, across countries and disciplines, in furthering our understanding of health, its determinants, and the impact of strategies aimed at addressing specific health issues.
A new study by Chang et al. reports that coronary artery bypass grafting (CABG) may be preferable to percutaneous coronary intervention (PCI) for multivessel coronary revascularization in appropriately selected patients on maintenance dialysis.
Hsu et al. report a progressive increase in the incidence of dialysis-requiring acute kidney injury (AKI) and associated deaths in the USA between 2000 and 2009. As with chronic kidney disease, a concerted campaign to increase awareness and alertness of AKI is urgently required. We must prevent “kidney attack”.
Podocytes, a key component of the glomerular filtration barrier, adhere tightly to the glomerular basement membrane (GBM) through the actions of extracellular ligands within the GBM, transmembrane podocyte adhesion receptors, and intracellular linker proteins. This Review summarizes recent advances in our understanding of the cell biology and genetics of podocyte adhesion with a focus on its functional relevance in physiology and disease.
Dysregulation of angiogenesis and tubulointerstitial hypoxia is a common finding in renal disease. In this Review, the authors describe the process of vascular remodelling and its regulation by angiogenic factors and inhibitors. They explain the mechanisms by which angiogenesis and hypoxia in the kidney might lead to progression of renal disease and discuss the potential advantages and disadvantages of angiogenic and anti-angiogenic therapies as well as novel strategies to stabilize and generate healthy vasculature.
Experimental, epidemiological and clinical studies have demonstrated that vasopressin contributes to the progression of chronic kidney disease by imposing an increased burden on diseased nephrons, and to autosomal dominant polycystic kidney disease by promoting cyst growth. Vasopressin also has a role in the pathogenesis of diabetes mellitus and metabolic disorders. This Review describes the adverse effects of vasopressin and provides insights into vasopressin physiology that may be relevant to the understanding of these adverse effects.
Variants in two neighbouring genes,APOL1 and MYH9, have previously been associated with kidney disease. Here, using 1000 genomes data, the authors reason by exclusion that the APOL1variants are in fact the most likely causal variants involved in kidney disease, and that this genomic region should be targeted in future studies to determine function.
