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Study Description

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.

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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
TypeSourcePlatformNumber of Oligos/SNPsSNP Batch IdComment
Whole Genome Genotyping Illumina HumanOmni1-Quad BeadChip N/A N/A
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Diseases/Traits Related to Study (MeSH terms)
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Study Attribution
  • Principal Investigator
    • Dan Roden, MD. Vanderbilt University Medical Center, Nashville, TN, USA.