Mariia White

ABSTRACT

Chronic kidney disease (CKD) is increasingly recognized as a systemic disorder that extends beyond renal impairment to influence gastrointestinal and neurological health. Disturbances in the gut microbial ecosystem promote the accumulation of protein-bound uremic toxins, including indoxyl sulfate (IS), p-cresyl sulfate (pCS), and trimethylamine N-oxide (TMAO), which have been implicated in vascular dysfunction and cerebrovascular injury. However, the mechanisms linking these metabolites to cerebral microhemorrhages remain incompletely understood. This study investigated the kidney–gut–brain axis using an adenine-induced murine model of CKD and a complementary cohort of patients receiving maintenance hemodialysis.