The number of hypotensive episodes during dialysis also correlates with the degree of frontal cerebral atrophy, a sequelae of recurrent strokes. Lipid and glucose control. Some observational studies have shown that statin therapy is associated with a decreased risk for cognitive impairment and dementia. However, more a recent large randomized controlled trial RCT suggested that statins given in late life to individuals at risk of vascular disease have no effect in preventing dementia. There is also no convincing evidence relating type or intensity of diabetic treatment to the prevention or management of cognitive impairment in Type II diabetes, even though epidemiological evidence shows a relationship between cognitive impairment and Type II diabetes.
Benefits and risks of tight glucose level control need to be assessed on an individual basis because of increased risks for hypoglycemia in CKD population. The small number of studies provide no consistent evidence either way that folic acid, with or without vitamin B12, has a beneficial effect on cognitive function of unselected healthy or cognitively impaired older people. The positive effect of oral folic acid on cognitive domains was found in participants with HCY and low vitamin B12 status after three years of follow-up.
However, homocysteine lowering with B- vitamin supplementation has failed to show benefit for reducing the risk of cognitive decline in the CKD population. Anti-oxidative therapy. Ginkgo biloba extract can be used as symptomatic treatment for cerebral insufficiency that occurs during normal aging or which may be due to degenerative dementia, vascular dementia or mixed forms, and for neurosensory disturbances.
There are no trials evaluating the effect of antioxidants on cognitive impairment in patients with CKD population. Exercise therapy. Many studies have shown an inverse relation between physical activity and the risk of developing cognitive decline in the elderly population. The cumulative meta-analysis to evaluate the role of physical activity on cognitive decline showed that subjects who performed a high level of physical activity were significantly protected against cognitive decline during the follow-up.
Furthermore, even low-to-moderate level exercise also showed a significant protection against cognitive impairment. Even though there is no study about effect of physical therapy on cognitive impairment in the CKD population, this is reliable therapy for patients with CKD due to the low risk of harm and many beneficial effects on muscle strength, work output, cardiac fitness, depressive symptoms and quality of life. In spite of beneficial effects of exercise in patients with CKD, there are currently no specific exercise guidelines for this population.
The exercise protocols currently available have often been developed for research studies and are therefore unsuitable for many chronically sick CKD patients with significant co-morbid conditions that need to be monitored. In view of local variations in treatment regimes, and variation in co-morbidities, exercise prescriptions for dialysis patients need to be tailored individually. Anemia treatment.. Anemia has also been identified as a risk factor for cognitive impairment in CKD, and correction of anemia with recombinant erythropoietin treatment has been shown to improve measures of cognition, such as neuropsychological and neurophysiological tests, in the several studies.
However, pretreatment hematocrit level was generally lower than current practice and post-treatment hematocrit was consistent with current clinical practice guidelines. In a small study of 20 HD patients, normalization of hematocrit from These results, however, need to be interpreted with caution because in the recent large RCTs of anemia in patients with CKD, normalization of hematocrit was associated with an increased risk for stroke, and increased risk for the composite outcome of death, myocardial infarction, hospitalization for congestive heart failure and no incremental improvement in quality of life.
Effect of frequent dialysis therapy. A small uncontrolled study showed that 12 patients who transitioned to daily nocturnal dialysis achieved improved cognitive outcomes in attention, psychomotor efficiency and processing speed, and working memory after 6 months. Although the mechanism by which daily dialysis can improve cognitive function remains unknown, it is suggested that improved toxin clearance and anemia, better control of blood pressure and parathyroid hormone, and less acute hemodynamic changes may be beneficial for the cerebral circulation and cognitive function.
Recent randomized clinical trials may give a more clear answer respecting the efficacy of frequent dialysis. Effects of renal transplantation. There are a few studies which cognitive function could improve following renal transplantation. In a recent short-term observational study, improvements in cognition in relation to baseline values were demonstrated 6 months after transplantation.
Prominent changes were evident with regard to memory, with minor improvements also noted in the domains of concentration and psychomotor function. Other groups have demonstrated improvements in both neuropsychological tests, such as the mini-mental state examination, and neurophysiological markers of cognitive function, as measured using evoked potential latencies and EEG rhythms.
However, in other study, significant residual impairment exists in transplant recipients compared with CKD patients. Pharmacologic therapy. They offer primarily symptomatic benefits, providing temporary cognitive improvement and deferred decline, but with little or no evidence of slowing disease progression. Galantamine, Rivastigmine, Donepezil and Memantine therapy for vascular or mixed dementia shows modest clinical benefits that are similar to those found for their treatment of AD, although these do not have FDA approval for this indication.
The pharmacokinetics of medications used to treat CKD patients require special consideration of the route of elimination, whether or not the medication is dialyzable and the protein binding of the medicine. Moreover, there is no published data on safety or efficacy of agents for dementia in CKD patients; thus, therapy decisions should be carefully individualized. Rivastigmine and Tacrine are mostly metabolized by liver, and very limited data suggest that no dose modification is probably required in these drugs.
Cognitive stimulation therapy CST. The pathogenesis appears complex, involving a variety of factors besides vascular disease - the most frequent trigger for 'standard' dementia in elderly people. Dialysis does not help or stop the process of cognitive decline, thus experts believe that factors which are not corrected completely by dialysis, for example the clearance of middle molecules, uncontrolled secondary hyperparathyroidism and anemia, may further the process of cognitive impairment.
The authors of the review emphasize that cognitive decline is one of many manifestations of brain damage that clearly accompany the decline of kidney function. Mark Findlay talking to us early on in the project in Necessary cookies are absolutely essential for the website to function properly.
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Non Necessary cookies to view the content. In the final days or weeks of life most people sleep. A common symptom of kidney failure is delirium. It develops because the toxins that are accumulating are affecting the brain. Usually the person must be kept in deep sleep, since mild sedation can worsen the confusion.
As hard as this is for family, it may be the only way to ensure a comfortable and calm final few hours or days. Conversation can be calming and meaningful for visitors and patients alike.
Pain is not common with kidney failure.
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