Methods: Clinical data from 9/1/2007 through 9/31/2015 were collected from the University of Kentucky Center for Clinical and Translational Science Enterprise Data Trust. Patients receiving SAM or PTZ for >48 hours were included. Patients were matched on: Charlson Comorbidity Index (CCI), baseline creatinine clearance, hypotension exposure, various nephrotoxic drug exposures, diagnosis of diabetes, heart failure, and hypertension. Basic descriptive statistics and multivariate regression were performed.
Results: Overall, 13,592 patient encounters were evaluated, with 612 and 12,980 receiving SAM and PTZ, respectively. On average, the PTZ group was slightly older (54 ± 17 vs 52 ± 15 years, p=0.0003), slightly less ill (CCI 3 [1-7] v 5 [2-9], p<0.00001), and had worse baseline creatinine clearance (91 [66-120] v 100 [78-128] mL/min, p<0.0001). AKI occurred in 2,934 (21.6%) patients in total, with 9.2% and 22.2% of SAM and PTZ patients experiencing AKI, respectively (p<0.00001). SAM patients were matched to 1836 PTZ patients. In the matched cohort 9.2% and 11.4% of SAM and PTZ patients experienced AKI, respectively (p=0.14). However, when VAN exposure is considered, the AKI rates are 8.9% SAM, 10.2% SAM+VAN, 9.5% PTZ, and 18.1% PTZ+VAN. After multivariate regression, receipt of PTZ+VAN was associated with an adjusted OR of 2.28 (95% CI 1.5-3.12, p <0.001) compared to PTZ alone. Whereas, receipt of SAM (p=0.56) or SAM+VAN (p=0.6) were not associated with increased odds of AKI.
Conclusion: AKI incidence was similar in patients treated with SAM and PTZ; however, the addition of VAN to PTZ significantly increased AKI incidence. This study demonstrates that the administration of multiple beta-lactam agents is not the likely mechanism for increased AKI observed with PTZ and VAN.
W. C. Rutter,