About this Research Topic
Chronic kidney disease (CKD) is a rising global health burden with an estimated prevalence worldwide of 11-13%. Prevalence rates increase to nearly 40% in persons aged 60+ years and it disproportionately affects those in low and middle Socio-demographic Index quintiles. CKD is associated with an eight- to ten-fold increase in cardiovascular mortality, equivalent to that in patients with diabetes or prior myocardial infarction, and even mild reductions in glomerular filtration rate (GFR; a measure of renal function) are associated with substantial increases in cardiovascular risk. There is a particularly strong association between CKD and cerebrovascular disease. Meta-analyses of cohort studies and trials indicate that reduced GFR is associated with a 40% greater risk of stroke by about 40% and that proteinuria is associated with a 70% greater risk even after adjusting for traditional cardiovascular risk factors. These associations may be attributable to a clustering of shared vascular risk factors including hypertension, diabetes mellitus, and atrial fibrillation but ‘non-traditional’ risk factors such as anemia, hyperuricemia, and mineral-bone disorders may also play a role.
Importantly, CKD also impacts cognitive brain health and is associated with a significant burden of cognitive impairment that worsens with declining renal function. Haemodialysis patients are three times more likely to have severe cognitive impairment than age-matched non-dialysis patients with reported prevalence rates of 30-40%. However, even early stages of CKD are associated with cognitive impairment. Mechanisms underlying the pathogenesis of cognitive impairment and dementia in CKD are poorly understood with both vascular and neurodegenerative hypotheses proposed. In support of the vascular hypothesis, there is a high prevalence of cardiovascular risk factors and a strong, blood-pressure-dependent association with stroke in CKD. However, CKD is also thought to augment potential neurodegenerative mechanisms through the interplay of hypertension and Alzheimer’s pathology. High concentrations of uraemic toxins such as neuroexcitatory guanidine compounds have also been implicated in CKD-related cognitive impairment as they have been found in strategic brain locations for cognition, such as the thalamus, mammillary bodies, and cerebral cortex. A better understanding of how CKD-generated toxins influence cognition has implications for treatment and prevention.
Original Articles, as well as Reviews of previously published literature, will be considered focusing mainly on the following topics:
· Acute cognitive disorders and the kidney
· Epidemiology and characteristics of cognitive impairment in CKD
· Mechanisms of cognitive dysfunction in CKD
· The impact of sleep disorders on cognitive function in CKD
· The impact of dialysis on cognitive brain health
· The clinical relevance of structural brain abnormalities in CKD
· Preventing and treating cognitive disorders in CKD
· Epidemiology, mechanisms, and outcomes of cognitive impairment in kidney transplant recipients
· The relationship between hypertensive disorders of pregnancy and cognitive brain health
· The impact of CKD on neurocognitive outcomes in children and adolescents
· Neuropsychiatric disorders in CKD
Importantly, CKD also impacts cognitive brain health and is associated with a significant burden of cognitive impairment that worsens with declining renal function. Haemodialysis patients are three times more likely to have severe cognitive impairment than age-matched non-dialysis patients with reported prevalence rates of 30-40%. However, even early stages of CKD are associated with cognitive impairment. Mechanisms underlying the pathogenesis of cognitive impairment and dementia in CKD are poorly understood with both vascular and neurodegenerative hypotheses proposed. In support of the vascular hypothesis, there is a high prevalence of cardiovascular risk factors and a strong, blood-pressure-dependent association with stroke in CKD. However, CKD is also thought to augment potential neurodegenerative mechanisms through the interplay of hypertension and Alzheimer’s pathology. High concentrations of uraemic toxins such as neuroexcitatory guanidine compounds have also been implicated in CKD-related cognitive impairment as they have been found in strategic brain locations for cognition, such as the thalamus, mammillary bodies, and cerebral cortex. A better understanding of how CKD-generated toxins influence cognition has implications for treatment and prevention.
Original Articles, as well as Reviews of previously published literature, will be considered focusing mainly on the following topics:
· Acute cognitive disorders and the kidney
· Epidemiology and characteristics of cognitive impairment in CKD
· Mechanisms of cognitive dysfunction in CKD
· The impact of sleep disorders on cognitive function in CKD
· The impact of dialysis on cognitive brain health
· The clinical relevance of structural brain abnormalities in CKD
· Preventing and treating cognitive disorders in CKD
· Epidemiology, mechanisms, and outcomes of cognitive impairment in kidney transplant recipients
· The relationship between hypertensive disorders of pregnancy and cognitive brain health
· The impact of CKD on neurocognitive outcomes in children and adolescents
· Neuropsychiatric disorders in CKD
Keywords: Chronic Kidney Disease, Proteinuria, Hypertension, Cognitive Impairment, Dementia
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