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Although most nephrologists spend their days managing patients with acute and chronic kidney disease (CKD), it is useful to occasionally consider the landscape of our current treatment approach. Here, we present the hypothesis that the major mechanisms that drive CKD are changing and will necessitate new approaches to manage this disease.

As IgA nephropathy (IgAN) is considered to result in part from autoimmune processes, B-cell depletion using rituximab might be a plausible therapy. However, a small randomized, controlled trial in patients at risk of progressive IgAN reports that this therapy failed to reduce proteinuria over 1 year and was associated with more adverse events per patient.

The degree to which systolic blood pressure should be lowered in individuals with mild hypertension is unclear. The Cardio-Sis trial has investigated whether tight systolic blood pressure control is more beneficial than usual control in individuals with hypertension but without diabetes.

Corticosteroids are frequently used to treat patients with IgA nephropathy (IgAN) despite a paucity of data to support their use in individuals with substantially reduced renal function. A retrospective study provides evidence that these agents may slow the rate of decline in renal function in high-risk patients with IgAN.

An epidemic of chronic kidney disease of unknown aetiology has emerged in Central America and resulted in the highest rates of end-stage renal disease worldwide. New findings from the first renal biopsy study of patients with Mesoamerican nephropathy should help medical detectives to 'crack' the cause of this disease.

Treatments administered to patients with primary IgA nephropathy (IgAN) and those with Henoch–Schönlein nephritis are largely based on opinion or weak evidence, and the recent KDIGO Clinical Practice Guidelines for Glomerulonephritis assigned low levels of evidence for the majority of recommendations and suggestions related to these two diseases. In this Review, Floege and Feehally describe an algorithm for structuring the treatment of IgAN depending on the clinical scenario, and discuss ongoing studies to investigate treatments.

A relationship between IgA nephropathy (IgAN) and the mucosa has long been recognized with evidence from clinical observations and genetic studies suggesting that abnormalities in the IgA mucosal immune system could be a key element in the pathogenesis of IgAN. In this Review, Jürgen Floege and John Feehally describe current evidence that links the mucosa, in particular the gastrointestinal mucosa, and IgA produced in the bone marrow with IgAN.

SGLT2 inhibitors have shown great promise in the management of diabetes mellitus and the prevention of cardiovascular complications, but increasing evidence suggests that their use can be associated with an increased risk of acute kidney injury. Insights into the mechanisms involved might help to identify individuals who are at risk of renal injury.

Aspirin and other antiplatelet agents are widely used in patients with chronic kidney disease. However, their use is often based on data obtained in patients with normal renal function. A recent Cochrane Collaboration systematic review analysed the benefits and risks of these agents in patients with chronic kidney disease.

Time-averaged proteinuria (TAP) is thought to be the most reliable predictor of outcomes in IgA nephropathy (IgAN). New data suggest that corticosteroids reduce TAP and presumably improve outcomes in IgAN, but increase the risk of adverse effects. Whether TAP is a good surrogate end point for clinical trials remains unclear.

In this Viewpoint, five members of theNature Reviews Nephrologyadvisory board reflect on the progress and frustrations of the past decade in basic and clinical nephrology research. They comment on areas where effort and money should be invested and the challenges that remain to be overcome, as well as give their predictions for progress in the next decade.

This Perspectives article considers why clinical trials of urate-lowering therapy (ULT) have shown inconsistent renoprotective effects in patients with chronic kidney disease, and suggests that sufficient evidence exists to support the use of routine screening for hyperuricaemia and initiation of ULT in selected patients.

Asymptomatic hyperuricaemia precedes and potentially contributes to the development of gout and other chronic diseases. This review summarizes what is known about the effects of uric acid on pro-inflammatory responses.

Recurrent dehydration and salt loss might be a mechanism that causes chronic kidney disease, whereby increased plasma osmolarity activates both intrarenal (polyol-fructokinase) and extrarenal (vasopressin) pathways to drive injury. The authors propose that water and salt influence blood pressure through the timing and combination of their intake, affecting plasma osmolarity and intrarenal and extrarenal mechanisms of renal injury.

Renal dendritic cells and macrophages are key factors in the initiation and propagation of renal disease and tissue regeneration. In this Review, the authors discuss the common and distinct characteristics of dendritic cells and macrophages as well as current understanding of the renal-specific functions of these important phagocytic, antigen-presenting cell types in potentiating or mitigating intrinsic kidney disease.