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End-stage renal disease (ESRD) disrupts erythrocyte deformability due to osmotic imbalances, oxidative stress, and uremic toxins, leading to impaired microcirculation and oxygen transport. Dysregulation of ion channels, particularly the Gardos channel, exacerbates dehydration and eryptosis, further compromising vascular integrity. Given the critical role of erythrocyte flexibility in oxygen delivery, this study investigates its relationship with aerobic capacity in ESRD patients, highlighting potential mechanisms of microvascular dysfunction
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End-stage renal disease (ESRD) profoundly alters osmotic homeostasis, disrupting erythrocyte deformability and impairing microcirculatory dynamics, ultimately compromising oxygen delivery to tissues. Persistent oxidative stress, hyperosmotic fluctuations, and accumulation of uremic toxins collectively modulate ion channel activity, particularly by stimulating cation influx and perturbing calcium regulation. These disruptions accelerate erythrocyte aging and promote eryptosis, a programmed form of red blood cell death. Furthermore, dysregulation of the Gardos channel exacerbates potassium efflux, leading to excessive cell dehydration, increased blood viscosity, and further deterioration of vascular integrity. Given the pivotal role of erythrocyte flexibility in oxygen transport efficiency, impairments in osmotic deformability may contribute to the reduced aerobic capacity frequently observed in ESRD patients. This study aims to elucidate the interplay between erythrocyte biomechanical properties and cardiopulmonary fitness in this population, shedding light on potential therapeutic targets to mitigate microvascular dysfunction.
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40 participants in 2 patient groups
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Jong-Shyan Wang, PhD
Data sourced from clinicaltrials.gov
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