• S Anathhanam and A J P Lewington.
• A Lewington, Department of Renal Medicine St James's University Hospital Leeds LS7 9JT, UK. andrew.lewington@leedsth.nhs.uk.
• J R Coll Physicians Edinb. 2013 Jan 1;43(4):323-8; quiz 329.

AbstractAcute kidney injury (AKI) represents a medical emergency associated with poor clinical outcomes. The international guideline group Kidney Disease: Improving Global Outcomes (KDIGO) has defined AKI according to rises in serum creatinine and/or reductions in urine output. Any patient who meets the criteria for AKI should be reviewed to ascertain the cause of AKI and the severity of the injury should be staged. Patients with more severe AKI are at greater risk of progression to chronic kidney disease (CKD). The 2009 National Confidential Enquiry into Patient Outcomes and Death (NCEPOD) reported that only 50% of patients who died with a diagnosis with AKI received good care. The mortality from AKI has remained unchanged for the last four decades and there are currently no specific therapies for the majority of cases of AKI. Patients with rarer forms of AKI need urgent renal referral for specific therapy. At present, serum creatinine and urine output remain the best biomarkers for detecting AKI. However, significant kidney damage has usually occurred by the time changes in these biomarkers are manifest and newer biomarkers are under investigation. Management of AKI is based upon general supportive measures, which includes treatment of the underlying cause and the initiation of renal replacement therapy (RRT) in patients with complications refractory to medical management. The optimal choice of intravenous fluid therapy remains controversial. There is currently renewed interest in more specific therapies for AKI secondary to hypoperfusion and/or sepsis, which have been previously unsuccessful. A number of therapeutic strategies are presently being explored in clinical trials.

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