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Objectives: Obesogenic medications are a putative contributor to the obesity epidemic. While 20% of adults take ≥1 obesogenic medication, the proportion in the end‐stage kidney disease (ESKD) population—a group enriched for cardiometabolic complications—is unknown. Obesogenic medications may contribute to obesity and hamper weight loss efforts to achieve transplant listing. Methods: Using 2017–2020 USRDS and Medicare claims, patients were identified as taking obesogenic medications if prescribed anticonvulsants, antidepressants, antidiabetics, anti‐inflammatories, antipsychotics, and/or antihypertensives known to cause weight gain for ≥30 days in their first hemodialysis year. Ordinal logistic and Cox regression with inverse probability of treatment weighting were used to quantify obesogenic medications' association with body mass index (BMI) and listing, respectively. Results: Among 271 401 hemodialysis initiates, 63.5% took ≥1 obesogenic medication. For those in underweight, normal weight, overweight, and class I, II, and III categories, 54.3%, 58.4%, 63.1%, 66.5%, 68.6%, and 68.8% took ≥1, respectively. Number of obesogenic medications was associated with increased BMI; use of one was associated with 13% increased odds of higher BMI (aOR [adjusted odds ratio] 1.14; 95%CI: 1.13–1.16; p < 0.001), use of three was associated with a 55% increase (aOR 1.55; 95%CI: 1.53–1.57; p < 0.001). Any use was associated with 6% lower odds of transplant listing (aHR [adjusted hazard ratio] 0.94; 95%CI: 0.92–0.96; p < 0.001). Within each BMI category, obesogenic medication use was associated with lower listing likelihood. Conclusions: Obesogenic medication use is common in ESKD patients—particularly those with obesity—and is associated with lower listing likelihood. Whenever possible, non‐obesogenic alternatives should be chosen for ESKD patients attempting weight loss to achieve transplant listing. [ABSTRACT FROM AUTHOR]

Background Frailty is associated with poor outcomes in surgical patients including kidney transplant (KT) recipients. Transplant centers that measure frailty have better pre- and postoperative outcomes. However, clinical utility of existing tools is low due to time constraints. To address this major barrier to implementation in the preoperative evaluation of patients, we developed an abridged frailty phenotype. Methods The abridged frailty phenotype was developed by simplifying the 5 physical frailty phenotype (PFP) components in a two-center prospective cohort of 3 220 KT candidates and tested for efficiency (time to completion) in 20 candidates evaluation (January 2009 to March 2020). We examined area under curve (AUC) and Cohen's kappa agreement to compare the abridged assessment with the PFP. We compared waitlist mortality risk (competing risks models) by frailty using the PFP and abridged assessment, respectively. Model discrimination was assessed using Harrell's C-statistic. Results Of 3 220 candidates, the PFP and abridged assessment identified 23.8% and 27.4% candidates as frail, respectively. The abridged frailty phenotype had substantial agreement (kappa = 0.69, 95% CI: 0.66–0.71) and excellent discrimination (AUC = 0.861). Among 20 patients at evaluation, abridged assessment took 5–7 minutes to complete. The PFP and abridged assessment had similar associations with waitlist mortality (subdistribution hazard ratio [SHR] = 1.62, 95% CI: 1.26–2.08 vs SHR = 1.70, 95% CI: 1.33–2.16) and comparable mortality discrimination (p  = .51). Conclusions The abridged assessment is an efficient and valid way to identify frailty. It predicts waitlist mortality without sacrificing discrimination. Surgical departments should consider utilizing the abridged assessment to evaluate frailty in patients when time is limited. [ABSTRACT FROM AUTHOR]

Direct‐acting antiviral (DAA) therapeutics have ushered in an era in which transplanting organs from donors infected with hepatitis C virus (HCV+) into recipients without (HCV–) is an increasingly common practice. Rare but potentially life‐threatening events have been reported in recipients of HCV+ organs. Since 2018 at our institution, 182 HCV– patients have received HCV+ donor organs. Here, we retrospectively reviewed cases in which recipients' family member caregivers reported sustaining needlestick exposures at home following discharge of the transplant recipient from the hospital. Caregiver needlestick exposures were passively reported in three cases of HCV+ into HCV– transplants (1.64% of such cases at our center). In all instances, the exposed individuals were aiding in diabetic management and the exposure occurred via lancets or insulin needles. In one case, the recipient viral load was undetectable at the time of the exposure but in the other two, recipients were viremic, putting their family members at risk to contract HCV infection. Surveillance for the exposed individuals was undertaken and no transmissions occurred. For centers performing HCV+ into HCV– transplants, it is important that informed consent includes discussion of potential secondary risks to family members and caregivers. Further, protocols for postexposure surveillance and for the acquisition of DAA treatment in the event of a secondary transmission should be in place. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2004.06.021 Byline: Rejji Kuruvilla (1), Larry S Zweifel (1), Natalia O Glebova (1), Bonnie E Lonze (1), Gregorio Valdez (2), Haihong Ye (1), David D Ginty (1) Abstract: A fundamental question in developmental biology is how a limited number of growth factors and their cognate receptors coordinate the formation of tissues and organs endowed with enormous morphological complexity. We report that the related neurotrophins NGF and NT-3, acting through a common receptor, TrkA, are required for sequential stages of sympathetic axon growth and, thus, innervation of target fields. Yet, while NGF supports TrkA internalization and retrograde signaling from distal axons to cell bodies to promote neuronal survival, NT-3 cannot. Interestingly, final target-derived NGF promotes expression of the p75 neurotrophin receptor, in turn causing a reduction in the sensitivity of axons to intermediate target-derived NT-3. We propose that a hierarchical neurotrophin signaling cascade coordinates sequential stages of sympathetic axon growth, innervation of targets, and survival in a manner dependent on the differential control of TrkA internalization, trafficking, and retrograde axonal signaling. Author Affiliation: (1) Department of Neuroscience, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, MD 21205 USA (2) Department of Neurobiology and Behavior, The State University of New York at Stony Brook, Stony Brook, NY 11794 USA Article History: Received 30 December 2003; Revised 21 May 2004; Accepted 1 June 2004 Article Note: (miscellaneous) Published: July 22, 2004