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- Study Description
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Important Links and Information
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- Instructions for requestors
- Data Use Certification (DUC) Agreement
- Talking Glossary of Genetic Terms
The goal of this study was to identify genetic variants associated with risk for acute kidney injury (AKI) in patients being treated with vancomycin and genetic variants associated with variability in vancomycin pharmacokinetics. AKI is a common adverse drug event and known complication of vancomycin therapy. Known risk factors fail to accurately predict renal toxicity. Our hypothesis, that genetic variants modify the risk of AKI, was tested by performing genome-wide association and linear regression in 555 patients of European descent using the outcome of peak serum creatinine while on vancomycin. We also tested the hypothesis that genetic variants associate with vancomycin pharmacokinetics, using vancomycin trough levels and calculated renal elimination rate constant as outcomes.
- Study Design:
- Prospective Longitudinal Cohort
- Study Type:
- Cohort
- dbGaP estimated ancestry using GRAF-pop
- Total number of consented subjects: 555
- Subject Sample Telemetry Report (SSTR)
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- Authorized Access
- Publicly Available Data
- Study Inclusion/Exclusion Criteria
All patients exposed to vancomycin with documented vancomycin dose, outcomes, and covariate data in BioVU, the Vanderbilt Biobank, were included. Children (age < 18 years), individuals who were not of European ancestry, and those failing quality control were excluded.
- Molecular Data
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Type Source Platform Number of Oligos/SNPs SNP Batch Id Comment Whole Genome Genotyping Illumina HumanOmni1-Quad BeadChip N/A N/A - Selected Publications
- Diseases/Traits Related to Study (MeSH terms)
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- Primary Phenotype: Acute Kidney Injury
- Authorized Data Access Requests
- Study Attribution
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Principal Investigator
- Dan Roden, MD. Vanderbilt University Medical Center, Nashville, TN, USA.
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Principal Investigator