3 research outputs found
Symptom Burden in Geriatric Hospitalized ESRD Patients: Quantifying symptoms to increase Nephrologist Awareness and use of Palliative Care Consultation
poster abstractBackground: End Stage Renal Disease (ESRD) patients have significant symptom burden. Reduced provider awareness of symptoms contributes to underutilization of symptom management resources.
Hypothesis: We hypothesize that improved nephrologist awareness of symptoms will lead to symptom improvement.
Methods: In this prospective, multicenter intervention study, 27 geriatric ESRD inpatients underwent symptom assessment using the modified Edmonton Symptom Assessment System (ESAS) at admission and 1 week post-discharge. Enrollees were sequentially randomized into 2 groups. In group 1, the nephrologist of each individual was provided baseline symptom assessment and not in group 2. Severity ratings were compared between in-hospital and post discharge scores as well as between the 2 groups.
Results: 26 patients completed the study; 1 died. There were no significant differences in baseline characteristics and scores, except increased diabetes in Group 2(P = 0.03). For 70% of the total cohort physicians reported not being surprised if the patient died within a year. Among the total cohort, total ESAS scores improved between initial and follow-up assessments except for depression, anxiety, lack of appetite and nausea. The absolute change in total ESAS scores was 10.9 in group1 and 6.8 in group2 (NS). Among individual symptoms significant improvement was found in pain and itching in group 1 only. Drowsiness and dyspnea improved in both groups. There was one palliative care consult.
Conclusions: Our findings reinforce the high symptom burden in geriatric ESRD patients. Residual symptoms post hospitalization and low utilization of palliative care resources is suggestive of a missed opportunity by nephrologists to address the high symptom burden at the inpatient encounter which is selective for sicker patients and/or inadequacy of dialysis to control these symptoms. The trend in improvement in pain and itching in group 1 may indicate better achievable symptom control if physician awareness is increased and simple pharmacological interventions are available
Implementation of a pharmacogenomics consult service to support the INGENIOUS trial
Hospital systems increasingly utilize pharmacogenomic testing to inform clinical prescribing. Successful implementation efforts have been modeled at many academic centers. In contrast, this report provides insights into the formation of a pharmacogenomics consultation service at a safety-net hospital, which predominantly serves low-income, uninsured, and vulnerable populations. The report describes the INdiana GENomics Implementation: an Opportunity for the UnderServed (INGENIOUS) trial and addresses concerns of adjudication, credentialing, and funding
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The chromatin landscape of healthy and injured cell types in the human kidney
There is a need to define regions of gene activation or repression that control human kidney cells in states of health, injury, and repair to understand the molecular pathogenesis of kidney disease and design therapeutic strategies. Comprehensive integration of gene expression with epigenetic features that define regulatory elements remains a significant challenge. We measure dual single nucleus RNA expression and chromatin accessibility, DNA methylation, and H3K27ac, H3K4me1, H3K4me3, and H3K27me3 histone modifications to decipher the chromatin landscape and gene regulation of the kidney in reference and adaptive injury states. We establish a spatially-anchored epigenomic atlas to define the kidney’s active, silent, and regulatory accessible chromatin regions across the genome. Using this atlas, we note distinct control of adaptive injury in different epithelial cell types. A proximal tubule cell transcription factor network of ELF3, KLF6, and KLF10 regulates the transition between health and injury, while in thick ascending limb cells this transition is regulated by NR2F1. Further, combined perturbation of ELF3, KLF6, and KLF10 distinguishes two adaptive proximal tubular cell subtypes, one of which manifested a repair trajectory after knockout. This atlas will serve as a foundation to facilitate targeted cell-specific therapeutics by reprogramming gene regulatory networks. © 2024, The Author(s).Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]