Acute Kidney Injury – An Update

Matt Varrier, Richard Fisher, *Marlies Ostermann

Department of Critical Care & Nephrology, Guy’s & St Thomas’ NHS Foundation Hospital, London, UK
*Correspondence to Marlies.Ostermann@gstt.nhs.uk

Disclosure: The authors have declared no conflicts of interest.
Received: 05.02.15 Accepted: 16.04.15
Citation: EMJ Nephrol. 2015;3[1]:75-82.

Abstract

The syndrome of acute kidney injury (AKI) occurs frequently in hospitalised patients, leading to increased morbidity, mortality, and healthcare expenditure. In the context of a precipitating insult, disturbances in both global and microcirculatory renal blood flow, tubular cell damage, and activation of pro- inflammatory pathways lead to impairment of numerous elements of renal function. Classification systems, including the recent ‘Kidney Disease: Improving Global Outcomes’ (KDIGO) classification, typically define and stage AKI in terms of the magnitude of rise in serum creatinine (SCr) and the presence of oliguria. At present there is no cure for AKI and the key principles of its management include early recognition, haemodynamic optimisation, correction of hypovolaemia, ceasing and avoidance of nephrotoxic medications, and treatment of the underlying cause. Recent data show that the type and volume of fluid therapy can affect renal function and that further guidance is required. In the future it is hoped that novel technologies, including biomarkers and real-time measurement of glomerular filtration rate will allow the earlier identification of patients with AKI, whilst a greater understanding of the pathogenesis of AKI will lead to the identification of new therapeutic targets. Despite SCr usually recovering after an episode of AKI, there is growing recognition that survivors of AKI are at an increased risk of subsequent chronic kidney disease, including end-stage renal failure and premature death.

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