Volume 10 Issue 12, December 2014

A new population-based study of a Norwegian registry containing data on more than 5 million individuals has confirmed the existence of powerful familial clustering of complex aetiologies of end-stage renal disease. Novel strategies for identifying additional nephropathy risk genes will benefit from such large familial registries.

A new study has reported a molecular signature of T-cell-mediated rejection in human kidney transplant biopsy samples that is enriched for effector T cells, interferon-γ and macrophages. Inhibitors of T-cell activation, such as CTLA4 and PDL1, were also prominent, raising the possibility that these immunological constrains could be harnessed by therapies for treating rejection.

A new study shows that statin therapy before diagnosis of diabetes mellitus is not associated with an increased risk of microvascular disease and might even be beneficial for retinopathy and neuropathy. These data suggest a potential protective effect of statins in specific complications, which should be further investigated in randomized controlled trials.

Desensitization therapy enables HLA-incompatible transplantation. However, desensitized patients have an increased risk of antibody-mediated rejection, and the presence of donor-specific antibodies (DSAs) is associated with poor outcomes. A new study has assessed the effect of rituximab induction on DSA production in kidney transplant recipients with high immunological risk.

FDA approval of the first device to use novel biomarkers of kidney damage to assess risk of acute kidney injury (AKI) potentially brings forward diagnosis of moderate-to-severe AKI to a time frame that could enable early intervention. Although the device awaits greater scrutiny, its approval marks the beginning of a new era.

Genetic studies have revealed a large number of gene mutations that can lead to the development of cystic kidney disease, but interpretation of genetic findings is complex and requires knowledge of differential diagnoses. This Review describes a clinical approach to the diagnosis of cystic kidney diseases on the basis of both kidney phenotype and extrarenal manifestations of the underlying disorder, in combination with genetic testing in selected patients.

Progression of kidney disease is characterized by the sustained release of proinflammatory and profibrotic cytokines and growth factors, leading to renal fibrosis. TGF-β is considered to be one of the main regulators of fibrosis, but preclinical studies have revealed important synergistic roles for other growth factors, including CTGF, EGF and PDGF, in this process. Here, the authors discuss the roles of these growth factors in kidney fibrosis, as well as the evidence supporting their qualification as additional targets for novel antifibrotic therapies.

Dietary interventions that aim to delay progression of chronic kidney disease (CKD) and decrease disease-associated mortality have a pivotal role in the management of CKD. Here, the authors discuss key studies that have investigated the effects of dietary salt, protein, fruits and vegetables, water and alcohol consumption in patients with CKD, and describe appropriate evidence-based dietary strategies that could prevent, or delay the progression of CKD.

Numerous studies have identified associations between gene polymorphisms and altered drug pharmacokinetics, particularly of immunosuppressive drugs used in solid organ transplantation. In this Review, Teun van Gelder and colleagues examine data supporting the ability of pharmacogenetic information to predict the pharmacokinetics or pharmacodynamics of immunosuppressive drugs, and discuss the potential impact of these data on clinical practice, with a focus on studies performed in renal transplant patients.

A prematurely aged phenotype is a common characteristic of chronic kidney disease (CKD) and other chronic organ diseases, including heart failure and rheumatoid arthritis. In this opinion article, the authors suggest four major pathophysiological mechanisms that may underlie premature ageing in CKD.