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Patients with chronic kidney disease (CKD) exhibit tremendously high levels of symptomatic and occult cerebrovascular disease and associated inflammatory factors, homocysteine, anemia, hypertension, and diabetes.1–4 As these risk factors overshadow aging and nonvascular factors, patients with CKD represent a potential model of accelerated vascular cognitive impairment.4
The brain and kidneys may be considered end organs on parallel trajectories, subject to shared cardiovascular risk factors, with microvascular pathologic processes mediated by inflammatory and oxidative processes taking place in similar low-resistance vascular beds and endothelial structures.4,5 Impaired endothelial function in the brain is manifested by defects in the blood-brain barrier and susceptibility to microinfarcts, lacunar infarcts, and white matter changes, and in the kidney by impaired glomerular filtration and secondary protein leakage, or proteinuria.5 Independently, the renal toxic effects of uremia, calcium-phosphate, other metabolic disturbances, and a potential genetic predisposition to exaggerated inflammatory response6 likely accelerate cognitive decline.
In this issue of Neurology®, Buchman et al.7 begin to unravel the convoluted relation between renal and cognitive impairment. Recent studies have described a graded, …
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