New approaches to acute kidney injury.

Acute kidney injury (AKI) is a common and serious clinical syndrome that involves complex interplay between different cellular, molecular, metabolic and immunologic mechanisms. Elucidating these pathophysiologic mechanisms is crucial to identify novel biomarkers and therapies. Recent innovative methodologies and the advancement of existing technologies has accelerated our understanding of AKI and led to unexpected new therapeutic candidates.

The microbiome and acute organ injury: focus on kidneys.

The microbiome of critically ill patients is significantly altered by both effects of the illnesses and clinical interventions provided during intensive care. Studies have shown that manipulating the microbiome can prevent or modulate complications of critical illness in experimental models and preliminary clinical trials. This review aims to discuss general concepts about the microbiome, including mechanisms of modifying acute organ dysfunction.

Lymphocytes and innate immune cells in acute kidney injury and repair.

Acute kidney injury (AKI) is a common and serious disease entity that affects native kidneys and allografts but for which no specific treatments exist. Complex intrarenal inflammatory processes driven by lymphocytes and innate immune cells have key roles in the development and progression of AKI. Many studies have focused on prevention of early injury in AKI.

Targeting immune cell glutamyl-prolyl-transfer RNA synthetase 1 (EPRS1) to prevent fibrosis after tubulointerstitial nephritis.

Glutamyl-prolyl-transfer RNA synthetase 1 is an enzyme that connects glutamic acid and proline to transfer RNA during protein synthesis. In this issue, a study by Kang et al. examined the role of the immune cell glutamyl-prolyl-transfer RNA synthetase 1 in toxin-induced tubulointerstitial nephritis mice.