Haemodialysis-related acute brain injury
While haemodialysis (HD) is a life-saving treatment for many people with chronic kidney disease (CKD), it inherently creates haemodynamic and osmotic stresses with potential for recurrent ischaemic injury to organs, including the brain. The most common brain injury is a rarefaction of white matter that is associated with long-term cognitive impairment of attention, memory and executive function. Despite progressive impairment being almost universal, the physiological mechanisms responsible for HD-induced brain injury are unclear.
The primary aim of this study was to examine the nature of acute HD-associated brain injury, and changes in brain structure and neurochemistry relevant to ischaemia, through anatomical MRI, diffusion tensor imaging and proton magnetic resonance spectroscopy. The secondary aim was to look for evidence of acute brain injury during a single HD session.
Participants with CKD (n=17; mean age 63 years) were randomised to receive either remote ischaemic preconditioning (RIPC) or sham intervention. Brain imaging was performed before HD treatment (pre-HD) and within the last 60 minutes of dialysis (late-HD) during maximal circulatory stress. Blood samples were taken pre-HD and at the end of HD, while blood pressure was measured pre-HD, at late-HD and at the end of HD.
A pattern of decrease of mean diffusivity and radial diffusivity was observed in multiple regions of white matter where fractional anisotropy increased from pre-HD to late-HD, a pattern attributed to cytotoxic oedema (with increase in global brain volumes). Additionally, intradialytic decreases in the brain metabolite N-acetyl aspartate and in choline were detected, indicating regional ischaemia.
The findings of intradialytic changes in brain tissue volume, diffusion metrics and brain metabolite concentrations are the first to demonstrate HD-induced brain injury occurring in a single dialysis session. The repeated delivery of HD could, therefore, have an impact on long-term structural brain injury and cognitive function.
The authors conclude that the prevention of brain injury and preservation of cognitive vitality must be a primary responsibility for those providing care to people on HD. The urgent further study of HD-induced brain injury, associated cognitive impairment and HD-directed interventions to mitigate the impact of HD on the brain (such as RIPC or dialysate cooling) is advocated.
The full study can be read here.
