Abstract: FR-PO013
Burden and Outcomes of Drug-Induced AKI
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
- Gudsoorkar, Prakash Shashikant, University of Cincinnati, Cincinnati, Ohio, United States
- Meganathan, Karthikeyan, University of Cincinnati, Cincinnati, Ohio, United States
- Sears, Amy, University of Cincinnati, Cincinnati, Ohio, United States
- Singleton, Evan P., University of Cincinnati, Cincinnati, Ohio, United States
- Kramer, Samantha M., University of Cincinnati, Cincinnati, Ohio, United States
- Harrison, Kathleen, University of Cincinnati, Cincinnati, Ohio, United States
- Thakar, Charuhas V., University of Cincinnati, Cincinnati, Ohio, United States
Background
Acute kidney injury (AKI) affects up to third of all hospitalizations. Although drug induced AKI (DI-AKI) is reported to be frequent, limited data exists in determining its true burden, and description of associated risk factors and outcomes.
Methods
All AKI consults (defined by KDIGO guidelines) across an academic health system were retrospectively recorded in an approved electronic registry. Of the available 500 cases of AKI (January to June 2018), 321 were studied (exclusion: kidney transplants, end stage renal disease, transfers on dialysis). AKI was classified by etiology on the day of consult as either nephrotoxic, biologic, or multifactorial; multifactorial was then scored (1 to 10 scale) based on contribution of the drug class. Drug induced (DI-AKI) was defined as either nephrotoxic or those with a multifactorial score > 5, and others as Biol-AKI. AKI was also classified as community acquired (CA-AKI), < 2 days or 2 or more days after admission (hospital acquired, HA-AKI), . The composite outcome was death, hospice discharge, dialysis dependence at discharge or 1.5 times median length of stay. Chi-square tests, and logistic regression were used for covariate adjustment (demographic, co-morbidities, and admission details).
Results
Of the 321 AKI cases (62% Male, 29% Black, median age 59 years, median baseline creatinine 1.3 mg/dl) DI-AKI occurred in 88 cases (27%). DI-AKI cases were more likely to be Black (40% vs 25%, p=0.01). Compared to Biol-AKI, DI-AKI admissions were mostly Medical (91% vs 78%, p=0.008). The most common drug classes associated with DI-AKI were diuretics 48%, antimicrobials 42%, renin-angiotensin system inhibitors 39%, contrast agents 30%, chemotherapy 7%. Most common source of DI-AKI was community acquired (64%). Need for dialysis was similar across two groups (DI-AKI - 22% vs Biol-AKI 34%). Overall, 50% of cases met the primary composite outcome [(DI-AKI – 38% vs Biol-AKI – 54%, p=0.008); risk-adjusted odds ratio (OR) 0.52 (95% CI, 0.31 – 0.86)].
Conclusion
Almost 1-in-3 AKI consults are drug induced, and attributable to commonly prescribed agents. Although Biol-AKI cases had a greater risk of composite outcome, DI-AKI cases continue to face devastating consequences, including similar risk of dialysis dependence. Strategies to mitigate drug induced AKI could improve clinical outcomes.