Adjudication of etiology of acute kidney injury: experience from the TRIBE-AKI multi-center study
1 Department of Internal Medicine, Program of Applied Translational Research, Yale University and Veterans Affairs Medical Center, 60 Temple Street, Suite 6C, New Haven, CT 06510, USA
2 Section of Nephrology, Department of Medicine, University of Chicago, Pritzker School of Medicine, Chicago, IL, USA
3 Department of Cardiothoracic Surgery, Danbury Hospital, Danbury, CT, USA
4 Division of Nephrology, Departments of Medicine, Epidemiology and Biostatistics, University of Western Ontario, London, ON, Canada
BMC Nephrology 2014, 15:105 doi:10.1186/1471-2369-15-105Published: 4 July 2014
Adjudication of patient outcomes is a common practice in medical research and clinical trials. However minimal data exists on the adjudication process in the setting of Acute Kidney Injury (AKI) as well as the ability to judge different etiologies (e.g. Acute Tubular Necrosis (ATN), Pre-renal Azotemia (PRA)).
We enrolled 475 consecutive patients undergoing cardiac surgery at four sites of the Translational Research Investigating Biomarker Endpoints in AKI (TRIBE-AKI) study. Three expert nephrologists performed independent chart review, utilizing clinical variables and retrospective case report forms with pre intra and post-operative data, and then adjudicated all cases of AKI (n = 67). AKI was defined as a > 50% increase in serum creatinine for baseline (RIFLE Risk). We examined the patterns of AKI diagnoses made by the adjudication panel as well as association of these diagnoses with pre and postoperative kidney injury biomarkers.
There was poor agreement across the panel of reviewers with their adjudicated diagnoses being independent of each other (Fleiss’ Kappa = 0.046). Based on the agreement of the two out of three reviewers, ATN was the adjudicated diagnosis in 41 cases (61%) while PRA occurred in 13 (19%). Neither serum creatinine or any other biomarker of AKI (urine or serum), was associated with an adjudicated diagnosis of ATN within the first 24 post-operative hours.
The etiology of AKI after cardiac surgery is probably multi-factorial and pure forms of AKI etiologies, such as ATN and PRA may not exist. Biomarkers did not appear to correlate with the adjudicated etiology of AKI; however the lack of agreement among the adjudicators impacted these results.