Supervised Exposure to XR Device-Task Configurations in Mild Cognitive Impairment: Descriptive Self-Report Acceptability Pilot Study.

Kidney diseases pose a major challenge to global public health systems. The spectrum of renal disorders is broad, ranging from common Chronic Kidney Disease (CKD) to acute and critical conditions such as acute Kidney Injury (AKI). All of these impose a heavy burden on human health and socioeconomic development. Among them, CKD has attracted particular attention due to its high prevalence (affecting approximately 9% of the global population) and significant associated disability and mortality (). CKD is not only an important risk factor for cardiovascular events but also a leading cause of end-stage renal disease, ultimately requiring costly renal replacement therapy to sustain life. Concurrently, the incidence of AKI among hospitalized patients can be as high as 20%. AKI itself carries a high mortality risk and is a critical event that accelerates the progression of CKD and worsens long-term prognosis (). A common feature underlying these diseases is that their onset and progression are closely intertwined with pathophysiological processes such as inflammation, oxidative stress, and disruption of internal homeostasis. Traditional perspectives in nephrology research have largely focused on pathological changes within the kidneys themselves. With the rapid advancement of microbiome science, it has become increasingly recognized that the human body functions as a complex ecosystem, in which interactions between distant organs play crucial roles in disease progression. Among these, the “gut-kidney axis” has emerged as a major focus in kidney disease research, with its pathophysiological significance becoming increasingly prominent (, ). The establishment of this theory is grounded in the following key evidence (): first, patients with kidney disease exhibit gut dysbiosis, characterized by a reduction in beneficial bacteria and their metabolites—such as short-chain fatty acids, an increase in opportunistic pathogens, and an overall decline in microbial diversity. Second, this dysbiotic gut microbiota compromises the integrity of the intestinal mucosal barrier, facilitating the translocation of endotoxins (e.g., lipopolysaccharide) and gut-derived uremic toxins (e.g., indoxyl sulfate, p-cresyl sulfate) into the systemic circulation (). Third, these gut-derived toxins exacerbate renal inflammation and oxidative stress, directly injuring kidney cells, and also activate systemic immune responses, thereby creating a vicious cycle of “gut toxin accumulation—systemic microinflammation—sustained deterioration of renal function.”