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Cerebral atrophy in patients on long-term regular hemodialysis treatment
Insights
Regular hemodialysis treatment (RDT) patients show high rates of cerebral atrophy, including cortical and subcortical damage. Factors like blood pressure and A1(OH)3 intake correlate with this brain damage.
Area of Science:
- Nephrology
- Neurology
- Radiology
Background:
- Chronic hemodialysis patients often experience neurological complications.
- Cerebral atrophy, encompassing cortical and subcortical damage, is a concern in long-term hemodialysis.
- The incidence and potential causes of cerebral atrophy in this population require further investigation.
Purpose of the Study:
- To investigate the prevalence of cerebral atrophy in patients undergoing regular hemodialysis treatment (RDT).
- To identify potential clinical and biochemical factors associated with cerebral atrophy in RDT patients.
Main Methods:
- Computed tomography (CT) scans were used to assess cerebral atrophy in 30 RDT patients and 50 controls.
- Clinical data including blood pressure, cholesterol, triglycerides, and A1(OH)3 intake were analyzed.
- Vascular calcification was assessed, and statistical correlations were performed using Fisher test and Discriminant Analysis.
Main Results:
- 46.6% of RDT patients exhibited cortical atrophy, while 16.6% showed subcortical atrophy.
- Cerebral atrophy showed a decreasing correlation with mean blood pressure, A1(OH)3 intake, blood cholesterol, arterial calcifications, and blood triglycerides.
- Subcortical atrophy was observed even without significant neurological symptoms.
Conclusions:
- Long-term regular hemodialysis treatment is associated with a high incidence of cerebral atrophy.
- Several clinical and biochemical parameters, including blood pressure and A1(OH)3 intake, are correlated with cerebral atrophy in RDT patients.
- Further research is needed to elucidate the causal mechanisms and implications of cerebral atrophy in hemodialysis patients.
Abstract:
The presence of Cerebral Atrophy in the form of cortical damage (Cortical Atrophy) or subcortical damage (enlargement of ventricular cavities) was explored by computed tomography (CT) scans in 30 patients maintained on regular hemodialysis treatment (RDT) for not less than 10 years, and less than 50 years of age. Whereas a group of 50 normal subjects of the same age, used as control, gave no evidence of cerebral atrophy, 46.6% of the patients maintained on RDT showed cortical atrophy, evenly diffuse in half the cases and predominantly frontal in the other half. In addition 16.6% of the patients showed subcortical atrophy, even in the absence of evident central neurologic or neuropsychic symptoms. In a search for the possible causes of this high incidence of cerebral atrophy in chronic hemodialysis patients we reviewed the last five years' profiles of clinical and blood biochemistry parameters known or suspected to produce brain damage when altered, as stored in a computer system available to our Hemodialysis Unit: these were mean blood pressure before and after hemodialysis, blood cholesterol and triglyceride assays, and mean daily oral intake of A1(OH)3. The status of arterial blood vessels in terms of vascular calcification in soft tissue roentgenograms was also defined; then we correlated these clinical and biochemical indices with the findings of cerebral CT scans by the Fisher test and Discriminant Analysis. The Fisher test revealed a decreasing correlation of cerebral atrophy with mean blood pressure, A1(OH)3 intake, blood cholesterol content, arterial calcifications and blood trygliceride assay in that order.(ABSTRACT TRUNCATED AT 250 WORDS)