Creating hemodialysis autogenous access in children and adolescents.

OBJECTIVE: End-stage renal disease (ESRD) in childhood and adolescence is rare, with relatively few published reports of pediatric ESRD vascular access. This study analyzes a 10-year experience creating arteriovenous fistulas (AVFs) in children and adolescents. Our goal is to review our strategy for creating functional autogenous vascular access in younger patients and report our results. METHODS: We retrospectively reviewed data and outcomes for consecutive vascular access patients aged ≤19 years during a 10-year period. Each patient had preoperative vascular ultrasound mapping by the operating surgeon in addition to physical examination. A distal forearm radiocephalic AVF was the first access choice when feasible, and a proximal radial artery inflow AVF was the next option. Demographic data, inflow artery, venous outflow target, and required transposition vs direct AVFs were variables included in the analysis. Primary and cumulative patency were calculated by Kaplan-Meier analysis. RESULTS: Thirty-seven AVFs were created in 35 patients. No grafts were used. Ages were 6 to 19 years (mean, 15 years), and 20 were male. Causes of ESRD included glomerular disease (n = 18) and urinary obstruction or reflux (n = 7), among others. Three had previous AVFs, and 10 were obese. The proximal radial artery supplied AVF inflow in 25 patients and the brachial artery in only seven. Eleven individuals required a transposition and one a vein translocation to the contralateral arm. No patients developed hand ischemia, although two later required banding procedures for high flow. Eleven patients had successful transplants. A single patient died, unrelated to the vascular access. Five AVFs failed. Of these, two had new successful AVFs created, two regained renal function, one was transplanted, and one declined other procedures. Primary and cumulative patency rates were 75% and 85% at 12 months, 70% and 85% at 24 months, and 51% and 85% at 36 months, respectively. Median follow-up was 16 months. CONCLUSIONS: Creating an AVF for hemodialysis is a successful vascular access strategy for pediatric and adolescent patients. Proximal radial artery AVFs provided safe and functional access when a distal AVF was not feasible. Cumulative AVF patency was 85% at 36 months.

The Geographic Distribution of Vascular Surgeons and Trainees by State in 2023.

OBJECTIVE: Approximately 1.4 vascular surgeons/100,000 persons are estimated to fulfill current patient needs in the United States (US), but an ongoing shortage exists. The aims of this study are to provide an updated nationwide state-by-state workforce analysis and compare the distribution of practicing vascular surgeons and training opportunities. METHODS: Vascular surgeons in the US were identified using the National Provider Identifier registry in 2023. Only board-certified and actively licensed vascular surgeons were included. To estimate the number of vascular surgery graduates per year in each state, integrated residency and fellowship-matched positions (trainees) were ascertained from the National Resident Matching Program website. Surgeons and trainees were totaled by state, and densities were calculated using the 2020 US Census Bureau state populations. These two cohorts were also examined together using simple linear regression and geographic mapping. RESULTS: This study included 3399 board-certified vascular surgeons and 228 newly matched trainees. The average densities of vascular surgeons and trainees in the US are 1/100,000 persons and 0.06/100,000 persons, respectively. The five states with the lowest densities of vascular surgeons are AR, ND, NV, OK, and WY, averaging 0.4/100,000 persons. Eight states (AK, ID, KS, ND, NM, NV, RI, WY) had zero training programs offering positions in 2023 and ranked in the lowest quartile for the number of practicing vascular surgeons (Figure 1). Simple linear regression demonstrated a statistically significant correlation between state rates of vascular surgeons and trainees (p < 0.001). CONCLUSION: States with zero training positions also have the fewest vascular surgeons per capita. Statewide attention to expanding vascular surgery training opportunities targeted in these areas could positively impact the current maldistribution and shortage of vascular surgeons.

NMDA receptor activation and calpain contribute to disruption of dendritic spines by the stress neuropeptide CRH.

The complex effects of stress on learning and memory are mediated, in part, by stress-induced changes in the composition and structure of excitatory synapses. In the hippocampus, the effects of stress involve several factors including glucocorticoids and the stress-released neuropeptide corticotropin-releasing hormone (CRH), which influence the integrity of dendritic spines and the structure and function of the excitatory synapses they carry. CRH, at nanomolar, presumed-stress levels, rapidly abolishes short-term synaptic plasticity and destroys dendritic spines, yet the mechanisms for these effects are not fully understood. Here we tested the hypothesis that glutamate receptor-mediated processes, which shape synaptic structure and function, are engaged by CRH and contribute to spine destabilization. In cultured rat hippocampal neurons, CRH application reduced dendritic spine density in a time- and dose-dependent manner, and this action depended on the CRH receptor type 1. CRH-mediated spine loss required network activity and the activation of NMDA, but not of AMPA receptors; indeed GluR1-containing dendritic spines were resistant to CRH. Downstream of NMDA receptors, the calcium-dependent enzyme, calpain, was recruited, resulting in the breakdown of spine actin-interacting proteins including spectrin. Pharmacological approaches demonstrated that calpain recruitment contributed critically to CRH-induced spine loss. In conclusion, the stress hormone CRH co-opts mechanisms that contribute to the plasticity and integrity of excitatory synapses, leading to selective loss of dendritic spines. This spine loss might function as an adaptive mechanism preventing the consequences of adverse memories associated with severe stress.