Abstract
Introduction: The incidence of acute kidney injury (AKI) related to vancomycin is variable, and several risk factors related to the treatment and patients may explain the nephrotoxicity. The role of urinary biomarkers in AKI related to vancomycin is unknown. Objective: The aim of this study was to evaluate the role of urinary IL-18, KIM-1, NGAL, TIMP-2, and IGFBP7 as diagnostic and prognostic predictors of AKI related to vancomycin. Methods: A prospective cohort study of patients receiving vancomycin and admitted to wards of a public university hospital from July 2019 to May 2020 was performed. We excluded patients that had AKI before starting vancomycin, hemodynamic instability, inability to collect urine, and chronic kidney disease stage 5. Results: Ninety-four patients were included, and the prevalence of AKI was 24.5%, while the general mortality was 8.7%. AKI occurred 11 ± 2 days after the first vancomycin dose. The most frequent KDIGO stage was 1 (61%). There was no difference between patients who developed and did not develop AKI due to gender, length of hospital stay, dose, and time of vancomycin use. Logistic regression identified age (OR 6.6, CI 1.16–38.22, p = 0.03), plasmatic vancomycin concentrations between 96 and 144 h (OR 1.18, CI 1.04-1.40, p = 0.04), and urinary NGAL levels between 96 and 144 h (OR 1.123, CI 1.096–1.290, p = 0.03) as predictors of AKI. The time of vancomycin use (OR 4.61, CI 1.11–22.02, p = 0.03), higher plasmatic vancomycin concentrations between 192 and 240 h (OR 1.02, CI 0.98–1.06, p = 0.26), and higher cell cycle arrest urinary biomarkers TIMP-2 multiplied by IGFBP-7 between 144 and 192 h (OR 1.33, CI 1.10–1.62, p = 0.02; OR 1.19, CI 1.09–1.39, p = 0.04, respectively) were identified as prognostic factors for non-recovery of kidney function at discharge. Conclusion: AKI related to vancomycin was frequent in patients hospitalized in wards. Age, plasmatic vancomycin concentrations, and NGAL between 96 and 144 h were identified as predictors of AKI related to vancomycin use. Plasmatic vancomycin concentrations and urinary NGAL were predictors of AKI diagnosis within the next 5 days. The urinary biomarkers of cell cycle arrest TIMP-2 and IGFBP-7 and the duration of vancomycin use were associated with non-recovery of kidney function at hospital discharge moment.
Highlights
The incidence of acute kidney injury (AKI) related to vancomycin is variable, and several risk factors related to the treatment and patients may explain the nephrotoxicity
This study aimed to evaluate the role of urinary biomarkers interleukin 18 (IL-18), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), tissue inhibitor of metalloproteinases 2 (TIMP-2), and IGFBP7 as diagnostic and prognostic predictors of AKI associated with vancomycin in hospitalized patients
Mean age was 51.1 ± 15.5 years, 67% were male, most of them had comorbidities (63.8%), and hypertension was the most frequent One hundred fourteen patients were excluded mainly due to present AKI before the introduction of vancomycin (81 patients) or due to difficulty in urine collection (Bagshaw et al, 2010) or need for noradrenalin (09 patients) or chronic kidney disease (CKD) stage 4 or 5
Summary
The incidence of acute kidney injury (AKI) related to vancomycin is variable, and several risk factors related to the treatment and patients may explain the nephrotoxicity. The main polemic points on vancomycin relate to its efficacy and safety. The incidence of vancomycin nephrotoxicity varies widely between different studies, reaching up to 40% and there are different factors related to the patient and/or the drug that can accelerate the nephrotoxicity. Among the factors associated with the patient, we highlight, mainly, advanced age, sepsis, dehydration, and reduced kidney function, while among the risk factors related to the drug are the concomitant administration with other drugs such as loop diuretics, amphotericin B, aminoglycosides, vasopressors, and intravenous contrast media; the longer duration of treatment and the high plasmatic vancomycin concentration (Elyasi et al, 2012; Zamoner et al, 2020)
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