%0 Journal Article
%T Diagnostic performance of fractional excretion of urea in the evaluation of critically ill patients with acute kidney injury: a multicenter cohort study
%A Michael Darmon
%A Francois Vincent
%A Jean Dellamonica
%A Frederique Schortgen
%A Frederic Gonzalez
%A Vincent Das
%A Fabrice Zeni
%A Laurent Brochard
%A Gilles Bernardin
%A Yves Cohen
%A Benoit Schlemmer
%J Critical Care
%D 2011
%I BioMed Central
%R 10.1186/cc10327
%X We conducted an observational, prospective, multicenter study at three ICUs in university hospitals. Unselected patients, except those with obstructive AKI, were admitted to the participating ICUs during a six-month period. Transient AKI was defined as AKI caused by renal hypoperfusion and reversal within three days. The results are reported as medians (interquartile ranges).A total of 203 patients were included. According to our definitions, 67 had no AKI, 54 had transient AKI and 82 had persistent AKI. FeUrea was 39% (28 to 40) in the no-AKI group, 41% (29 to 54) in the transient AKI group and 32% (22 to 51) in the persistent AKI group (P = 0.12). FeUrea was of little help in distinguishing transient AKI from persistent AKI, with the area under the receiver operating characteristic curve being 0.59 (95% confidence interval, 0.49 to 0.70; P = 0.06). Sensitivity was 63% and specificity was 54% with a cutoff of 35%. In the subgroup of patients receiving diuretics, the results were similar.FeUrea may be of little help in distinguishing transient AKI from persistent AKI in critically ill patients, including those receiving diuretic therapy. Additional studies are needed to evaluate alternative markers or strategies to differentiate transient from persistent AKI.Acute kidney injury (AKI) is common and associated with high mortality in critically ill patients [1-3]. The causes of AKI other than urinary tract obstruction are usually divided into two categories: prerenal causes, in which low renal perfusion leads to promptly reversible renal dysfunction, and intrinsic causes with renal tissue damage and persistent renal dysfunction. Although pathological studies are lacking, the leading cause of persistent AKI in critically ill patients is believed to be acute tubular necrosis (ATN) [4,5]. It is usually assumed that there is a continuum that leads from prerenal AKI to ATN [4-6]. Many publications in the fields of internal medicine, nephrology and critical care still advoca
%K acute kidney failure
%K ICU
%K fractional excretion of sodium
%K acute tubular necrosis
%K diuretics
%K sensitivity and specificity
%U http://ccforum.com/content/15/4/R178