Antibiotic-associated acute kidney injury (AA-AKI) is quite common, especially among hospitalized patients; however, little is known about risk factors or mechanisms of why AA-AKI occurs. In this review, the authors have reviewed all available literature prior to 1 June 2022, with a large number of AKI reports. Information regarding risk factors of AA-AKI, mechanisms behind AA-AKI, and treatment/management principles to decrease AA-AKI risk were collected and reviewed. Patients treated in the inpatient setting are at increased risk of AA-AKI due to common risk factors: hypovolemia, concomitant use of other nephrotoxic medications, and exacerbation of comorbid conditions. Clinicians should attempt to correct risk factors for AA-AKI, choose antibiotic therapies with decreased association of AA-AKI to protect their high-risk patients, and narrow, when clinically possible, the use of antibiotics which have decreased incidence of AKI. To treat AKI, it is still recommended to discontinue all offending nephrotoxic agents and to renally adjust all medications according to package insert recommendations to decrease patient harm.

Vancomycin-associated acute kidney injury (AKI) is a popular topic in the medical literature with few clear answers. While many studies evaluate the risk of AKI associated with vancomycin, few data are high quality and/or long in duration of follow-up. This review takes the clinician through an approach to evaluate a patient for risk of AKI. This evaluation should include patient assessment, antibiotic prescription, duration, and monitoring. Patient assessment involves evaluating severity of illness, baseline renal function, hypotension/vasopressor use, and concomitant nephrotoxins. Evaluation of antibiotic prescription includes evaluating the need for methicillin-resistant Staphylococcus aureus (MRSA) coverage and/or vancomycin use. Duration of therapy has been shown to increase the risk of AKI. Efforts to de-escalate vancomycin from the antimicrobial regimen, including MRSA nasal swabs and rapid diagnostics, should be used to lessen the likelihood of AKI. Adequate monitoring includes therapeutic drug monitoring, ongoing fluid status evaluations, and a continual reassessment of AKI risk. The issues with serum creatinine make the timely evaluation of renal function and diagnosis of the cause of AKI problematic. Most notably, concomitant piperacillin-tazobactam can increase serum creatinine via tubular secretion, resulting in higher rates of AKI being reported. The few studies evaluating the long-term prognosis of AKI in patients receiving vancomycin have found that few patients require renal replacement therapy and that the long-term risk of death is unaffected for patients surviving after the initial 28-day period.

No consensus exists regarding optimal dosing of norepinephrine in septic shock. We aimed to evaluate if weight-based dosing (WBD) lead to higher norepinephrine doses when achieving goal mean arterial pressure (MAP) than non-weight-based dosing (non-WBD). This was a retrospective cohort study conducted after standardization of norepinephrine dosing within a cardiopulmonary ICU. Patients received non-WBD prior to standardization (November 2018–October 2019) and WBD afterwards (November 2019–October 2020). The primary outcome was the norepinephrine dose needed to attain goal MAP. Secondary outcomes included time to goal MAP, duration of norepinephrine therapy, duration of mechanical ventilation, and treatment-related adverse effects. A total of 189 patients were included (WBD 97; non-WBD 92). There was a significantly lower norepinephrine dose at goal MAP (WBD 0.05, IQR 0.02, 0.07; non-WBD 0.07, IQR 0.05, 0.14; p < 0.005) and initial norepinephrine dose (WBD 0.02, IQR 0.01, 0.05; non-WBD 0.06, 0.04, 0.12; p < 0.005) in the WBD group. No difference was observed in achievement of goal MAP (WBD 73%; non-WBD 78%; p = 0.09) or time until goal MAP (WBD 18, IQR 0, 60; non-WBD 30, IQR 14, 60; p = 0.84). WBD may lead to lower norepinephrine doses. Both strategies achieved goal MAP with no significant difference in time to goal.

Pharmacists are essential healthcare providers but historically are not well represented as principal investigators (PIs) of R01 grants by the United States (US) National Institutes of Health (NIH). Pharmacy organizations have taken steps to provide pharmacists with research training to improve their chances of achieving PI status. We conducted a retrospective cohort study using data from the NIH RePORTER website about R01 grants awarded to PIs affiliated with US Schools of Pharmacy (SOPs) for the fiscal years 2005–2019. Information regarding professional degrees was supplemented using data from the PIs’ institutional website profiles and other internet-based sources. Only doctorate degrees obtained within the US were included for clinically related degrees. Data regarding more than one year of funding for the same project, equipment supplements, and diversity supplements were excluded to focus on unique projects in year one of funding. PhDs were the primary unique PIs of R01 grants at US SOPs (>90%). Pharmacist representation as unique PIs increased over the 15 years but was still only 10.1% for the years 2015–2019. There was a higher percentage of female pharmacists as unique PIs than female non-pharmacists. Pharmacists are currently underrepresented as unique PIs for NIH R01 grants. This conclusion is limited by not knowing how many pharmacist R01 applications were submitted.

(1) Background: Excessive intravenous therapy (EIV) is associated with negative consequences, but guidelines are unclear about when switching to oral therapy is appropriate. (2) Methods: This cohort included patients aged ≥18 years receiving ≥48 h of antimicrobial therapy for bacteremia due to Escherichia coli, Pseudomonas aeruginosa, Enterobacter, Klebsiella, Acinetobacter, or Stenotrophomonas maltophilia from 1/01/2008–8/31/2011. Patients with a polymicrobial infection or recurrent bacteremia were excluded. Potential EIV (PEIV) was defined as days of intravenous antibiotic therapy beyond having a normal WBC count for 24 h and being afebrile for 48 h until discharge or death. (3) Results: Sixty-nine percent of patients had PEIV. Patients who received PEIV were more likely to receive intravenous therapy until discharge (46 vs. 16%, p < 0.001). Receipt of PEIV was associated with a longer mean time to receiving oral antimicrobials (8.7 vs. 3 days, p < 0.001). The only factors that impacted EIV days in the multivariable linear regression model were the source of infection (urinary tract) (coefficient −1.54, 95%CI −2.82 to −0.26) and Pitt bacteremia score (coefficient 0.51, 95%CI 0.10 to 0.92). (4) Conclusions: PEIV is common in inpatients with Gram-negative bacteremia. Clinicians should look to avoid PEIV in the inpatient setting.