Jay L Koyner1, Steven G Coca2, Heather Thiessen-Philbrook3, Uptal D Patel4, Michael G Shlipak5, Amit X Garg3, Chirag R Parikh6. 1. Section of Nephrology, Department of Medicine, University of Chicago, Pritzker School of Medicine, Chicago, IL. 2. Department of Internal Medicine, Clinical Epidemiology Research Center, Yale University School of Medicine, New Haven, CT. 3. Division of Nephrology, Department of Medicine, University of Western Ontario, London, Ontario, Canada. 4. Duke University, School of Medicine, Durham, NC. 5. Division of General Internal Medicine, San Francisco VA Medical Center, University of California, San Francisco, CA. 6. Department of Internal Medicine, Clinical Epidemiology Research Center, Yale University School of Medicine, New Haven, CT. Electronic address: chirag.parikh@yale.edu.
Abstract
BACKGROUND: The interaction between baseline kidney function and the performance of biomarkers of acute kidney injury (AKI) on the development of AKI is unclear. STUDY DESIGN: Post hoc analysis of prospective cohort study. SETTING & PARTICIPANTS: The 1,219 TRIBE-AKI Consortium adult cardiac surgery cohort participants. PREDICTOR: Unadjusted postoperative urinary biomarkers of AKI measured within 6 hours of surgery. OUTCOME: AKI was defined as AKI Network stage 1 (any AKI) or higher, as well as a doubling of serum creatinine level from the preoperative value or the need for post-operative dialysis (severe AKI). MEASUREMENTS: Stratified analyses by preoperative estimated glomerular filtration rate (eGFR) ≤ 60 versus > 60mL/min/1.73m(2). RESULTS: 180 (42%) patients with preoperative eGFRs≤60mL/min/1.73m(2) developed clinical AKI compared with 246 (31%) of those with eGFRs>60mL/min/1.73m(2) (P<0.001). For log2-transformed biomarker concentrations, there was a significant interaction between any AKI and baseline eGFR for interleukin 18 (P=0.007) and borderline significance for liver-type fatty acid binding protein (P=0.06). For all biomarkers, the adjusted relative risk (RR) point estimates for the risk for any AKI were higher in those with elevated baseline eGFRs compared with those with eGFRs≤60mL/min/1.73m(2). However, the difference in magnitude of these risks was low (adjusted RRs were 1.04 [95% CI, 0.99-1.09] and 1.11 [95% CI, 1.07-1.15] for those with preoperative eGFRs≤60mL/min/1.73m(2) and those with higher eGFRs, respectively). Although no biomarker displayed an interaction for baseline eGFR and severe AKI, log2-transformed interleukin 18 and kidney injury molecule 1 had significant adjusted RRs for severe AKI in those with and without baseline eGFRs≤60mL/min/1.73m(2). LIMITATIONS: Limited numbers of patients with severe AKI and post-operative dialysis. CONCLUSIONS: The association between early postoperative AKI urinary biomarkers and AKI is modified by preoperative eGFR. The degree of this modification and its impact on the biomarker-AKI association is small across biomarkers. Our findings suggest that distinct biomarker cutoffs for those with and without a preoperative eGFR≤60mL/min/1.73m(2) is not necessary. Published by Elsevier Inc.
BACKGROUND: The interaction between baseline kidney function and the performance of biomarkers of acute kidney injury (AKI) on the development of AKI is unclear. STUDY DESIGN: Post hoc analysis of prospective cohort study. SETTING & PARTICIPANTS: The 1,219 TRIBE-AKI Consortium adult cardiac surgery cohort participants. PREDICTOR: Unadjusted postoperative urinary biomarkers of AKI measured within 6 hours of surgery. OUTCOME: AKI was defined as AKI Network stage 1 (any AKI) or higher, as well as a doubling of serum creatinine level from the preoperative value or the need for post-operative dialysis (severe AKI). MEASUREMENTS: Stratified analyses by preoperative estimated glomerular filtration rate (eGFR) ≤ 60 versus > 60mL/min/1.73m(2). RESULTS: 180 (42%) patients with preoperative eGFRs≤60mL/min/1.73m(2) developed clinical AKI compared with 246 (31%) of those with eGFRs>60mL/min/1.73m(2) (P<0.001). For log2-transformed biomarker concentrations, there was a significant interaction between any AKI and baseline eGFR for interleukin 18 (P=0.007) and borderline significance for liver-type fatty acid binding protein (P=0.06). For all biomarkers, the adjusted relative risk (RR) point estimates for the risk for any AKI were higher in those with elevated baseline eGFRs compared with those with eGFRs≤60mL/min/1.73m(2). However, the difference in magnitude of these risks was low (adjusted RRs were 1.04 [95% CI, 0.99-1.09] and 1.11 [95% CI, 1.07-1.15] for those with preoperative eGFRs≤60mL/min/1.73m(2) and those with higher eGFRs, respectively). Although no biomarker displayed an interaction for baseline eGFR and severe AKI, log2-transformed interleukin 18 and kidney injury molecule 1 had significant adjusted RRs for severe AKI in those with and without baseline eGFRs≤60mL/min/1.73m(2). LIMITATIONS: Limited numbers of patients with severe AKI and post-operative dialysis. CONCLUSIONS: The association between early postoperative AKI urinary biomarkers and AKI is modified by preoperative eGFR. The degree of this modification and its impact on the biomarker-AKI association is small across biomarkers. Our findings suggest that distinct biomarker cutoffs for those with and without a preoperative eGFR≤60mL/min/1.73m(2) is not necessary. Published by Elsevier Inc.
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