Acute kidney injury: new studies
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Antoine G. Schneider Rinaldo Bellomo
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Acute kidney injury: new studies
Received: 24 January 2013 Accepted: 28 January 2013 Published online: 16 February 2013 Ó Springer-Verlag Berlin Heidelberg and ESICM 2013 A. G. Schneider R. Bellomo ()) Intensive Care Unit, Austin Health, 145 Studley Road, Heidelberg, Melbourne, VIC 3084, Australia e-mail: [email protected] Tel.: ?61-3-94965992 Fax: ?61-3-94963932 A. G. Schneider e-mail: [email protected] A. G. Schneider R. Bellomo Australian and New Zealand Research Centre, Monash University, Melbourne, VIC, Australia
Acute kidney injury (AKI) is common in critically ill patients and independently associated with important morbidity and mortality [1]. However, its pathophysiology and optimal management remain largely unknown. In this brief review, we present recent advances in the understanding, prevention and management of AKI.
Biomarkers In the last decade, several molecules have been identified as potential early biomarkers of renal injury [2–4]. A growing body of evidence suggests that, at least in some subgroups of patients, these biomarkers may allow earlier and, perhaps, more sensitive identification of AKI than current creatinine-based diagnostic criteria. In particular, a recent multicentre prospective cohort study [5]
aimed to determine the diagnostic performance of several urinary biomarkers [neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), interleukin (IL)-18, liver-type fatty acid binding protein and cystatin C] to predict AKI when obtained in the emergency department (1,635 unselected patients). After exclusion of patients with minimal creatinine rise and rapid (\72 h) renal recovery, all biomarkers were elevated in patients with AKI. Urinary NGAL was found to be the most specific (81 %) and sensitive (68 %) biomarker (cut-off 104 ng/ml) and to have good discriminatory ability for AKI. All tested biomarkers were found to have excellent negative predictive value ([95 %). Models including KIM-1 or urinary NGAL improved patient reclassification by more than 20 % as compared with creatinine-based models. Similar analyses performed in 380 cardiac surgery patients with post-operative AKI showed that three biomarkers (urinary IL-18, urinary albumin-to-creatinine ratio and urinary and plasma NGAL) were useful in predicting AKI progression [6]. Each biomarker was able to improve risk stratification and to identify patients at risk for progression of AKI, with plasma NGAL performing the best. Altogether, these data confirm previous findings in similar populations [7, 8]. Further studies are still required to determine the clinical utility of renal biomarkers in heterogeneous critically ill patients. However, renal-specific biomarkers have already improved our understanding of the pathophysiology of AKI. This is illustrated by another study, which challenged the concept of ‘‘pre-renal’’ AKI [9]. In 529 patients with measurements obtained at 0, 12 and 24 h following intensive ca
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