Abstract: FR-PO014
Drug-Induced AKI: Can We Prevent It?
Session Information
- AKI: Epidemiology, Risk Factors, Prevention - II
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Sears, Amy, University of Cincinnati, Cincinnati, Ohio, United States
- Harrison, Kathleen, University of Cincinnati, Cincinnati, Ohio, United States
- Gudsoorkar, Prakash Shashikant, University of Cincinnati, Cincinnati, Ohio, United States
- Meganathan, Karthikeyan, University of Cincinnati, Cincinnati, Ohio, United States
- Kramer, Samantha M., University of Cincinnati, Cincinnati, Ohio, United States
- Singleton, Evan P., University of Cincinnati, Cincinnati, Ohio, United States
- Thakar, Charuhas V., University of Cincinnati, Cincinnati, Ohio, United States
Background
Acute kidney injury (AKI) can affect 1-in-3 hospitalizations, with an adverse impact on both patients and health systems. AKI is far too commonly drug induced (DI_AKI). Limited data exists in identifying whether DI_AKI can be prevented, and whether patient or provider interventions could improve kidney safety.
Methods
We studied all inpatient nephrology consults with AKI (defined by KDIGO guidelines) at two centers across our academic health system between January and June of 2018. Based on a prior quality improvement program, AKI cases were retrospectively adjudicated to be Biologic (Biol_AKI) or Drug Induced (DI_AKI). We further identified DI_AKI as Preventable (Prv_AKI) when the use of the culprit drug(s) was not considered to be of life-saving value for diagnosis or treatment. Source of AKI was defined as community acquired (CA_AKI = AKI criteria met < 2 days of admission) or hospital acquired (HA_AKI). A composite outcome was hospital death, discharge to hospice or dialysis dependence on discharge. Chi-square tests were used for comparison.
Results
Of the 500 AKI consults, 321 were studied (exclusion: kidney transplants, end stage renal disease, transfers on dialysis). DI_AKI occured in 27% (88/321), and was deemed preventable (Prv_AKI) in 24/88 (27%) of cases. Prv_AKI cases were 63% Men, 54% Black (median age 60.5 years; median baseline creatinine 1.3 mg/dl) Prv_AKI predominantly occurred in Medical settings (96%), and admissions for sepsis or cardiovascular causes comprised 50% of all cases. The top two drug classes associated with Prv_AKI were diuretics (63%) and Renin-Angiotensin System (RAS) blockers (54%). For non-Prv_AKI cases, anti-microbial use (50%) and diuretics (42%) were the top two offending drug classes. Contrast agents were third common class for both groups. Source of AKI in the Prv_AKI group was CA_AKI 54% vs HA_AKI 46% and not significantly different with non-Prv_AKI group (p=0.26). The composite outcome was similar in Prv_AKI (38%) and non-Prv_AKI (38%) groups.
Conclusion
Almost third of drug induced AKI can be preventable, and the majority of these AKI cases manifest within 2 days of admission. Preventable AKI cases faced the same devastating outcome as their counterparts. These findings suggest that patient or provider education about medication safety could improve clinical outcomes in AKI.
Funding
- Clinical Revenue Support