Abstract
Background
The incidence and impact of adverse drug events (ADEs) leading to hospitalization
and as a predominant risk factor for late graft loss has not been studied in transplantation.
Methods
This was a longitudinal cohort study of adult kidney recipients transplanted between
2005 and 2010 and followed through 2013. There were 3 cohorts: no readmissions, readmissions
not due to an adverse drug event, and adverse drug events contributing to readmissions.
The rationale of the adverse drug events contribution to the readmission was categorized
in terms of probability, preventability, and severity.
Results
A total of 837 patients with 963 hospital readmissions were included; 47.9% had at
least one hospital readmission and 65.0% of readmissions were deemed as having an
ADE contribute. The predominant causes of readmissions related to ADEs included non-opportunistic
infections (39.6%), opportunistic infections (10.5%), rejection (18.1%), and acute
kidney injury (11.8%). Over time, readmissions due to under-immunosuppression (rejection)
significantly decreased (−1.6% per year), while those due to over-immunosuppression
(infection, cancer, or cytopenias) significantly increased (2.1% increase per year
[difference 3.7%, P = .026]). Delayed graft function, rejection, creatinine, graft loss, and death were
all significantly greater in those with an ADE that contributed to a readmission compared
the other two cohorts (P < .05).
Conclusion
These results demonstrate that ADEs may be associated with a significant increase
in the risk of hospital readmission after kidney transplant and subsequent graft loss.
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Article info
Publication history
Published online: November 22, 2017
Accepted:
September 26,
2017
Footnotes
Supported through grants from the National Institute of Diabetes and Digestive under Award numbers K23DK099440 and T35DK007431 and from the Agency for Healthcare Research and Quality under award number R18HS023754.
Presented at the 12th Annual Academic Surgical Congress in Las Vegas, NV, February 7–9, 2017.
Identification
Copyright
© 2017 Elsevier Inc. All rights reserved.