Acute kidney injury

Acute kidney injury (AKI) is a rapid deterioration in kidney function that occurs within 48 hours of an initiating event and is associated with an absolute increase in serum creatinine of ≥26.4 μmol/l. Main causes of AKI include sepsis, ischaemia-reperfusion injury and nephrotoxins. Symptoms include fatigue, loss of appetite, headache, nausea and vomiting.

Latest Research and Reviews

News and Comment

  • News and Views |

    The analyses in the 2017 Global Burden of Disease Study demonstrate the growing burden of chronic kidney disease (CKD), mainly driven by population ageing; absolute levels for every CKD metric considered rose significantly, whereas age-standardized rates were fairly stable. The prevalence of key metabolic CKD risk factors, particularly obesity, also show a worrying increase.

    • Simon D. S. Fraser
    •  & Paul J. Roderick
  • News and Views |

    New findings demonstrate that endothelial nitric oxide synthase regulates major metabolic pathways in the kidney proximal tubule, which confers protection against oxidative stress during acute kidney injury (AKI). These findings give new insights into AKI pathophysiology and nitric oxide biology, and identify new targets for the treatment of AKI.

    • Pierre-Yves Martin
    •  & Sophie de Seigneux
  • News and Views |

    Peritoneal dialysis has many advantages over haemodialysis in the treatment of acute kidney injury (AKI) in low-resource settings. One limitation, however, is the availability of commercial dialysis fluid. Following the International Society of Peritoneal Dialysis AKI guidelines, a frontline hospital in Cameroon now shows that locally prepared fluids are safe and effective.

    • Simon J. Davies
  • Comments and Opinion |

    Numerous exciting studies that advanced our understanding of immune-mediated kidney disease were published in 2018. Whereas most of these studies analysed the role of pro-inflammatory mediators, several novel anti-inflammatory mechanisms were discovered that involve immune cells and mediators with previously unrecognized protective roles in renal disease.

    • Christian Kurts
    •  & Catherine Meyer-Schwesinger