IntroductionVancomycin 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 materialsA 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.ResultsA 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)ConclusionsModerate 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.

Pediatric pulmonary hypertension (PAH) is a rare disease that carries a poor prognosis if left untreated. Although there are published guidelines for the treatment of children with pulmonary hypertension, due to the limited number of robust pediatric clinical trials, recommendations are often based on limited data or clinical experience. Furthermore, many practical aspects of care, particularly for the pediatric patient, are learned through experience and best navigated with a multidisciplinary team. While newer PAH therapies have been approved for adults, there is still limited but expanding experience in pediatrics. This new information will help improve the targets of goal‐oriented therapy. Lastly, this review highlights practical aspects in the use of the different therapies available for the treatment of pediatric pulmonary hypertension.

Respiratory infections caused by non‐tuberculous mycobacteria (NTM) are a major cause of morbidity for patients living with cystic fibrosis (CF), as NTM pulmonary disease (NTM‐PD) is challenging to both diagnose and eradicate. Despite the lengthy courses of the established regimens recommended by the Cystic Fibrosis Foundation (CFF) and European Cystic Fibrosis Society (ECFS) consensus guidelines, only about 50% to 60% of patients achieve culture conversion, and treatment regimens are often complicated by antibiotic resistance and toxicities. Since publication of the CFF/ECFS guidelines, several new or alternative antibiotic regimens have been described for patients with CF who have NTM‐PD. These regimens offer new options for patients who do not clear NTM with standard therapies or cannot utilize the usual regimens due to toxicities or drug‐drug interactions.

To the Editor, Airway mucus dehydration from loss of cystic fibrosis transmembrane conductance regulator (CFTR) activity leads to excessive airway muco-inflammation that drives the onset and progression of lung disease in cystic fibrosis (CF.) 1,2 Previous studies with the highly effective modulator therapy (HEMT) ivacaftor have demonstrated improvement in CFTR function and substantial clinical benefits. However, clinical studies of ivacaftor therapy in people with CF (PwCF) with eligible genotypes have not consistently demonstrated a significant reduction in markers of airway inflammation. 3,4 This somewhat unanticipated result suggests that airway inflammation may persist in PwCF on HEMT and could benefit from anti-inflammatory therapies.Recently, elexacaftor-tezacaftor-ivacaftor (ETI, Trikafta) was approved as a HEMT available to a larger fraction of PwCF. While in vitro evidence suggests that ETI treatment may alter inflammatory pathways in CF, 5 there is little information regarding the impact of ETI on airway inflammation in treated individuals. To address this issue, we identified PwCF who underwent bronchoscopy with bronchoalveolar lavage (BAL) after starting ETI therapy. To avoid confounding by indication, the study population was limited to those who had surveillance procedures before and after starting ETI therapy. BAL markers of inflammation and infection obtained during these procedures were then compared.