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Rationale: Acute kidney injury is a common and severe complication of critical illness and cardiac surgery. Despite significant attempts at developing treatments, therapeutic advances to attenuate acute kidney injury and expedite recovery have largely failed.Objectives: Identifying genetic loci associated with increased risk of acute kidney injury may reveal novel pathways for therapeutic development.Methods: We conducted an exploratory genome-wide association study to identify single-nucleotide polymorphisms associated with genetic susceptibility to in-hospital acute kidney injury.Measurements and Main Results: We genotyped 609,508 single-nucleotide polymorphisms and performed genotype imputation in 760 acute kidney injury cases and 669 controls. We then evaluated polymorphisms that showed the strongest association with acute kidney injury in a replication patient population containing 206 cases with 1,406 controls. We observed an association between acute kidney injury and four single-nucleotide polymorphisms at two independent loci on metaanalysis of discovery and replication populations. These include rs62341639 (metaanalysis P = 2.48 × 10-7; odds ratio [OR], 0.64; 95% confidence interval [CI], 0.55-0.76) and rs62341657 (P = 3.26 × 10-7; OR, 0.65; 95% CI, 0.55-0.76) on chromosome 4 near APOL1-regulator IRF2, and rs9617814 (metaanalysis P = 3.81 × 10-6; OR, 0.70; 95% CI, 0.60-0.81) and rs10854554 (P = 6.53 × 10-7; OR, 0.67; 95% CI, 0.57-0.79) on chromosome 22 near acute kidney injury-related gene TBX1.Conclusions: Our findings reveal two genetic loci that are associated with acute kidney injury. Additional studies should be conducted to functionally evaluate these loci and to identify other common genetic variants contributing to acute kidney injury. [ABSTRACT FROM AUTHOR]

Objective: To determine whether preoperative aspirin-acetylsalicylic acid (ASA)-timing or dose independently affects 30-day all-cause mortality. Background: Preoperative ASA administration is associated with reduced morbidity and mortality after coronary artery bypass graft (CABG). However, data are lacking regarding optimal timing and dosing of ASA. Methods: We retrospectively reviewed data from 3018 consecutive patients who underwent CABG surgery between July 2005 and May 2011. Patients were assigned to 3 groups according to the time of the last preoperative ASA dose: (1) 24 hours or less preoperatively (n=1173), (2) between 24 and 72 hours (n=876), and (3) more than 72 hours or none (n=969). In a separate analysis, patients were grouped according to ASA dose: 81mg (n=1285), 325mg (n=1004), and none (n=543). The primary outcome was 30-day allcause mortality. Results: The 30-day mortality rate was significantly lower in patients who took ASA 24 hours or less preoperatively (1.5%) than in those who took it between 24 and 72 hours (3.2%) or more than 72 hours or none (2.9%). Multivariate analysis showed that ASA within 24 hours preoperatively was associated with reduced mortality (odds ratio [OR], 0.41; 95% confidence interval [CI], 0.20-0.82; P=0.01). Moreover, mortality was significantly reduced for patients taking 81mg of ASA (1.4%) compared with 325mg (2.9%) or none (3.9%). Multivariate analysis demonstrated that 81mg of ASA decreased mortality risk by 66% (OR, 0.34; 95% CI, 0.18-0.66; P<0.01), whereas 325mg of ASA had no mortality benefit (OR, 0.74; 95% CI, 0.41- 1.35; P=0.33) compared with no ASA. Conclusions: Low-dose ASA use within 24 hours of CABG is independently associated with decreased early postoperative mortality. [ABSTRACT FROM AUTHOR]