Extracorporeal hemoadsorption and neurological disorders: A challenging perspective

Extracorporeal hemoadsorption is a promising therapeutic strategy for neurological complications associated with chronic kidney disease and acute kidney injury. Neurological disorders—including cognitive impairment, Parkinson disease, and dementia—are more prevalent in individuals with renal dysfunction due to shared inflammatory pathways and the accumulation of protein-bound uremic toxins (PBUTs), such as advanced glycation end products (AGEs), indoxyl sulfate, and p-Cresol. PBUTs exacerbate neurological conditions by promoting neuroinflammation and neurodegeneration. They are inadequately removed via conventional dialysis, necessitating alternative solutions. Hemoadsorption has shown potential in reducing systemic inflammation and eliminating PBUTs, offering neuroprotective and disease-modifying effects. Preclinical studies have demonstrated significant reductions in AGEs, indoxyl sulfate, and amyloid-beta peptides in models of Alzheimer’s disease (AD) and other conditions, improving outcomes. In clinical trials involving inflammatory disorders such as Guillain-Barré syndrome, hemoadsorption reduced cytokines—including tumor necrosis factor alpha, interleukin-17 (IL-17), and IL-22—correlating with enhanced recovery and reduced ventilation requirements. While evidence supports its efficacy, further research is needed to standardize protocols, evaluate long-term outcomes, and explore its potential in broader populations. Hemoadsorption could transform the management of individuals with renal and neurological disorders, improving disease outcomes and quality of life.