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MUSE (microscopy with UV surface excitation) image of fixed unsectioned kidney, showing a renal artery with elastic lamina surrounded by collagen with renal tubules on either side. Cover image supplied by Richard Levenson, Department of Pathology and Laboratory Medicine, University of California Davis Medical Center at Sacramento, California, USA.
New research supports the notion that pre-renal and intrinsic acute kidney injury are distinct molecular entities and hence different disease states despite similar increases in serum creatinine level. Pre-renal AKI induces protective molecular mechanisms whereas intrinsic AKI requires a 'second hit' that upregulates injury genes, and results in a persistent elevation of serum creatinine and kidney injury biomarkers.
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.
Acute kidney injury continues to challenge physicians, researchers and patients. To date, there is no efficient treatment for acute kidney injury and its occurrence in many critically ill patients seems inevitable. However, a new study might just change the way we approach this seemingly intractable problem.
Decreasing susceptibility to tissue damage — a protective strategy known as tolerance — might be as important as infection resistance in determining outcomes in sepsis. Here, the authors discuss tolerance mechanisms that act in the kidney during sepsis, with a focus on the role of metabolic reprogramming.
Regular physical activity is associated with reduced mortality in the general population and in patients with chronic kidney disease. Here, the authors discuss the importance of physical activity for patients with renal disease and patient-reported barriers and facilitators for physical activity.
Contrast agents can damage the kidney through several mechanisms. Here, the authors discuss current understanding of the incidence and pathophysiology of contrast-induced acute kidney injury and highlight the need to consider individual patient risk factors when considering prevention strategies.
Here, five leading researchers describe changes in the epidemiology of obesity-related kidney disease, advances in current understanding of the mechanisms involved and current approaches to the management of affected patients.