Dataset Information

Vancomycin associated acute kidney injury in pediatric patients.

ABSTRACT: INTRODUCTION:Vancomycin associated acute kidney injury (vAKI) is a well known complication in pediatric patients. Identification and characterization of the incidence and risk factors for vAKI in the pediatric population would assist clinicians in potentially preventing or mitigating vAKI. METHODS AND MATERIALS:A 6 year retrospective cohort study was designed. Patients were included if they were < 19 years of age, received vancomycin as inpatients, and had a baseline SCr and one other SCr drawn during and up to 72 hours after the discontinuation of vancomycin. Data collection included patient demographics, vancomycin doses and length of therapy, vancomycin serum concentrations, and concomitant medications. The Kidney Disease Improving Global Outcomes (KDIGO) criteria were used to characterize acute kidney injury. Descriptive statistical methods were used and ordinal logistic regression was employed to determine variables significantly associated with vAKI. RESULTS:A total of 7,095 patients met study criteria (55.4% male, median age 4.1 years (IQR 0.67-11.2 years)). Mechanical ventilation was used in 7.9% (n = 563) and mortality was 4.9% (n = 344). A total of 153 concomitant medications were identified. A median of 5 (IQR 3-7) SCr values were obtained and median SCr prior to vancomycin was 0.39 (IQR 0.28-0.57) mg/dL (CrCl 134±58 mL/min/1.73m2). Vancomycin was administered for a median of 2 (IQR 1-3) days (14.9±1.6 mg/kg/dose). vAKI was present in 12.2% (n = 862: KDIGO stage 1 (8.30%, n = 589), KDIGO stage 2 (1.94%, n = 138) KDIGO stage 3 (1.89%, n = 134)). Mean vancomycin serum concentration at 6-8 hours after a dose for patients with vAKI (10.7±8.9 mg/L) was significantly, but not clinically different for patients with no vAKI (7.5±6.3 mg/L). (p<0.05) Ordinal logistic regression identified total dose of vancomycin, vancomycin administration in the intensive care unit, and concomitant medication administration as significant for vAKI. In particular, concomitant administration of several different medications, including nafcillin, clindamycin, and acetazolamide, were noted for strong associations with vAKI. (p<0.05). CONCLUSIONS:Moderate to severe acute kidney injury due to vancomycin is infrequent in children and associated with concomitant medication use and total dose of vancomycin. Serum vancomycin concentrations are not useful predictors of vAKI in the pediatric population.

SUBMITTER: Moffett BS

PROVIDER: S-EPMC6169857 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Vancomycin associated acute kidney injury in pediatric patients.

Moffett Brady S BS Morris Jennifer J Kam Charissa C Galati Marianne M Dutta Ankhi A Akcan-Arikan Ayse A

PloS one 20181003 10

<h4>Introduction</h4>Vancomycin associated acute kidney injury (vAKI) is a well known complication in pediatric patients. Identification and characterization of the incidence and risk factors for vAKI in the pediatric population would assist clinicians in potentially preventing or mitigating vAKI.<h4>Methods and materials</h4>A 6 year retrospective cohort study was designed. Patients were included if they were < 19 years of age, received vancomycin as inpatients, and had a baseline SCr and one o ...[more]

PMID: 30281600

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Project description:The objective of this study was to investigate the current situation of vancomycin (VAN)-associated acute kidney injury (VA-AKI) in China and identify the risk factors for VA-AKI, as well as to comprehensively examine the risk related to concurrent drug use. Further, we assessed the outcomes of patients who developed VA-AKI and the risk factors for these outcomes. Finally, we aimed to provide suggestions for improving the prevention and treatment of VA-AKI in China.We conducted a retrospective observational study of inpatients who had been treated with VAN between January 2013 and December 2013 at Peking University First Hospital. AKI was defined as an increase in SCr of ?0.3 mg/dl (?26.5 ?mol/l) within 48 hours or an increase to ?1.5 times the baseline certainly or presumably within the past 7 days. VA-AKI was defined as the development of AKI during VAN therapy or within 7 days following the termination of VAN therapy. In addition, we compared patients with NO-AKI, who did not develop AKI during their hospitalization, with those with VA-AKI.Of the 934 patients treated with VAN during their hospital stay, 740 were included in this study. Among those excluded, 38.1% (74/194) were excluded because of a lack of data on serum creatinine (SCr). Among the included patients, 120 had confirmed VA-AKI, with an incidence of 16.2% (120/740). Multiple logistic regression analysis revealed that an elevated baseline estimated glomerular filtration rate (eGFR) (odds ratio [OR] = 1.009; p = 0.017) and concomitant vasopressor therapy (OR = 2.942; p = 0.009), nitrate use (OR = 2.869; p = 0.007), imipenem-cilastatin treatment (OR = 4.708; p = 0.000), and contrast medium administration (OR = 6.609 p = 0.005) were independent risk factors for VA-AKI; in addition, the receipt of orthopedic/trauma/burn surgery (OR = 0.3575; p = 0.011) and concomitant compound glycyrrhizin use (OR = 0.290; p = 0.017) were independent protective factors for VA-AKI. Multiple logistic regression analysis also demonstrated that among the patients who developed VA-AKI, coronary heart disease (CHD) (OR = 12.6; p = 0.006) and concomitant vasopressor therapy (OR = 15.4; p = 0.001) were independent risk factors for death. We also evaluated the factors influencing improvement of renal function. Multiple logistic regression analysis demonstrated that CHD (OR = 8.858, p = 0.019) and concomitant contrast medium administration (OR = 9.779, p = 0.005) were independent risk factors and that simultaneous ?-blocker treatment (OR = 0.124, p = 0.001) was an independent protective factor for improvement of renal function.Patients treated with VAN received insufficient monitoring of SCr and inadequate therapeutic drug monitoring. We recommend that hospitals increase their investment in clinical pharmacists. An elevated baseline eGFR and concomitant vasopressor therapy, nitrate use, imipenem-cilastatin treatment, and contrast medium administration were independent risk factors for VA-AKI; in addition, orthopedic/trauma/burn surgery and concomitant compound glycyrrhizin use were independent protective factors for VA-AKI.

Project description:Vancomycin has been associated with acute kidney injury (AKI). However, the pharmacokinetic/toxicodynamic relationship for AKI is not well defined. Allometrically scaled vancomycin exposures were used to assess the relationship between vancomycin exposure and AKI. Male Sprague-Dawley rats received clinical-grade vancomycin in normal saline (NS) as intraperitoneal (i.p.) injections for 24- to 72-h durations with doses ranging 0 to 200 mg/kg of body weight divided once or twice daily. Urine was collected over the protocol's final 24 h. Renal histopathology was qualitatively scored. Urinary biomarkers (e.g., cystatin C, clusterin, kidney injury molecule 1 [KIM-1], osteopontin, lipocalin 2/neutrophil gelatinase-associated lipocalin 2) were assayed using a Luminex xMAP system. Plasma vancomycin concentrations were assayed by high-performance liquid chromatography with UV detection. A three-compartment vancomycin pharmacokinetic model was fit to the data with the Pmetrics package for R. The exposure-response in the first 24 h was evaluated using Spearman's nonparametric correlation coefficient (rs) values for the area under the concentration-time curve during the first 24 h (AUC0-24), the maximum concentration in plasma during the first 24 h (Cmax0-24 ), and the lowest (minimum) concentration in plasma after the dose closest to 24 h (Cmin0-24 ). A total of 52 rats received vancomycin (n = 42) or NS (n = 10). The strongest exposure-response correlations were observed between AUC0-24 and Cmax0-24 and urinary AKI biomarkers. Exposure-response correlations (rs values) for AUC0-24, Cmax0-24 , and Cmin0-24 were 0.37, 0.39, and 0.22, respectively, for clusterin; 0.42, 0.45, and 0.26, respectively, for KIM-1; and 0.52, 0.55, and 0.42, respectively, for osteopontin. However, no differences in histopathological scores were observed. Optimal sampling times after administration of the i.p. dose were 0.25, 0.75, 2.75, and 8 h for the once-daily dosing schemes and 0.25, 1.25, 14.5, and 17.25 h for the twice-daily dosing schemes. Our observations suggest that AUC0-24 or Cmax0-24 correlates with increases in urinary AKI biomarkers.

Dataset Information

Vancomycin associated acute kidney injury in pediatric patients.

Publications

Vancomycin associated acute kidney injury in pediatric patients.

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