Volume 9 Issue 2, February 2013

The year 2012 brought a continued harvest of new findings of relevance to glomerular biology and disease. Progress in glomerular disease has continued, although our understanding of disease processes continues to extend much further than our ability to intervene effectively.

During 2012, an observational study confirmed the high risk of cardiovascular disease ascribed to chronic kidney disease (CKD) and again raised the question of whether CKD should be considered a cardiovascular disease risk equivalent. Several other studies evaluated methods to mitigate cardiovascular risk in CKD. The results of these studies have advanced the field but have also raised more questions.

2012 saw the classification of the systemic vasculitides revised. Genetic studies showed that granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) are different diseases with aberrant immune responses to different autoantigens. B-cell depletion with rituximab also acquired a primary role in the treatment of GPA and MPA, as well as in cryoglobulinaemic vasculitis.

2012 saw the publication of four important trials investigating the choice of fluid therapy in patients suffering from critical illness or undergoing major surgery. These studies pave the way for more evidence-based administration of fluid in such patients.

Patients with end-stage renal disease typically receive three 3–4 h haemodialysis sessions per week. Although available data from well-powered randomized trials are limited, studies published in 2012 provided new evidence that haemodialysis regimens with longer treatment times and/or a higher frequency of sessions might reduce the high morbidity and mortality of patients on maintenance dialysis.

In the past few years, basic research and epidemiological studies have provided a wealth of new data on renal prognosis following acute kidney injury (AKI) and the potential association of AKI with incident chronic kidney disease (CKD), progression of CKD, and incident end-stage renal disease. The authors of this Review describe these findings and discuss the possible mechanisms by which AKI might lead to CKD or CKD progression.

This Review discusses the concept of Ras-related C3 botulinum toxin substrate 1 (Rac1)-induced activation of the mineralocorticoid receptor and highlights the available evidence for the roles of Rac1 and mineralocorticoid-receptor activation in cardiac and renal disease. The authors suggest that agents that regulate the activity of the Rac1-mineralocorticoid-receptor pathway could be novel therapeutic candidates for the treatment of chronic kidney disease and cardiac injury.

Heart failure and renal dysfunction frequently coexist. The term cardiorenal syndrome (CRS) is frequently used to describe this scenario, but the definition of CRS has been a matter of debate and has evolved over time. Here, the authors review the concept of CRS and its evolution and classification, and describe current and future targets for the clinical management of CRS. In addition, they propose a new classification system with seven distinct categories.

Blockade of the renin-angiotensin-aldosterone system (RAAS) is a standard treatment for patients with chronic kidney disease (CKD). Intensive strategies with single-agent or dual-agent RAAS blockade have been used to reduce proteinuria and blood pressure in these patients. This Review discusses strategies for improving the long-term outcomes of patients with CKD treated with RAAS blockade, focusing on the effects of combined low-dietary sodium intake and RAAS-blockade on the risk of renal and cardiovascular outcomes.