From the Guidelines
Vancomycin-induced acute kidney injury (AKI) typically develops within 5-7 days after starting treatment, though it can occur as early as 2-3 days or as late as 2 weeks into therapy. The risk of AKI increases with higher trough concentrations (especially >20 mg/L), longer treatment duration (>7 days), and higher daily doses (>4g/day) 1. Patients with pre-existing kidney disease, older age, or those receiving concurrent nephrotoxic medications are at higher risk. Vancomycin causes AKI through direct proximal tubular toxicity, oxidative stress, and mitochondrial damage.
Some key points to consider when using vancomycin include:
- Regular monitoring of kidney function (serum creatinine) and vancomycin levels is recommended, particularly during the first week of therapy 1.
- Maintaining appropriate trough levels (10-15 mg/L for most infections, 15-20 mg/L for severe infections) can help minimize kidney injury risk 1.
- The bactericidal activity of vancomycin is AUC 24h/MIC-dependent, and AUC 24h cannot be monitored routinely, but it correlates with residual concentration, which should therefore be measured 1.
- In discontinuous administration, the residual concentration must be determined before administration of the fourth dose, and the target for residual concentration or steady-state concentration in continuous infusion is around 20 mg/L 1.
If AKI develops, it's typically reversible with prompt discontinuation or dose adjustment of vancomycin, though complete recovery may take days to weeks. It's essential to weigh the benefits of vancomycin therapy against the potential risks of AKI, especially in patients with pre-existing kidney disease or those receiving concurrent nephrotoxic medications 1.
From the FDA Drug Label
The mean elimination half-life of vancomycin from plasma is 4 to 6 hours in subjects with normal renal function. In the first 24 hours, about 75% of an administered dose of vancomycin is excreted in urine by glomerular filtration. Renal dysfunction slows excretion of vancomycin. The FDA drug label does not answer the question.
From the Research
Vancomycin and Acute Kidney Injury (AKI)
- The time it takes for vancomycin to cause AKI is not explicitly stated in the provided studies, but several factors contribute to the risk of AKI, including serum vancomycin levels, concurrent nephrotoxic medications, and vasopressor therapy 2, 3.
- A study found that vancomycin use is associated with a higher risk of AKI when serum levels exceed 20 mg/L 2.
- Another study reported that vancomycin-associated AKI occurred in 40% of critically ill adolescent and young adult patients, with higher vancomycin trough levels, concurrent nephrotoxic agents, and concurrent vasopressor therapy increasing the risk of AKI 3.
- A systematic review and meta-analysis suggested that vancomycin treatment is associated with a higher risk of AKI, with a relative risk of 2.45 (95% confidence interval, 1.69 to 3.55) 4.
- A study on mice found that the time of administration of vancomycin affects the induction of AKI, with macrophages playing a role in the difference 5.
Risk Factors for Vancomycin-Associated AKI
- High vancomycin trough levels (> 20 mg/L) 2
- Concurrent nephrotoxic medications 3
- Concurrent vasopressor therapy 3
- Undergoing a procedure while on vancomycin 3
- Time of administration of vancomycin 5