Urine albumin-creatinine ratio, eGFR linked with structural brain damage across etiology
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Researchers identified a correlation between eGFR and urine albumin-creatinine ratio with structural brain damage across various regions of etiology, according to data published in the American Journal of Kidney Diseases.
Further, the findings suggest that Alzheimer’s disease (AD) and limbic-predominant age-related TDP-43 encephalopathy (LATE) might not be significant contributors to neurodegeneration associated with chronic kidney disease.
“Previous studies have reported an association of kidney function measures with brain atrophy, cerebrovascular pathologies and white matter abnormalities, but characterized the brain damage as primarily driven by vascular causes and its nature as being functional rather than structural,” Johannes B. Scheppach, MD, from the department of epidemiology at Bloomberg School of Public Health at Johns Hopkins University, and colleagues wrote. They added, “Our aim was to examine whether the association of these kidney function measures with brain MRI abnormalities differs for pathologies that are usually associated with Alzheimer’s disease and LATE compared to those typically related to vascular dementia.”
In a cross-sectional study, researchers evaluated kidney function and albuminuria in 1,527 participants from the Atherosclerosis Risk in Communities (ARIC) Study between 1987 and 1989. The ARIC study included individuals aged 45 to 64 years. Those with evidence of cognitive impairment and a stratified random sample were invited for a brain MRI scan at the fifth study visit.
This study focused on white and African American participants with data for brain MRI, eGFR, urine albumin-creatinine-ratio (UACR) and covariates. Researchers examined brain images for brain micro-hemorrhages and infarcts.
Researchers sought to determine if the correlation between eGFR and brain MRI changes differed based on which markers were used for the estimation of GFR. For example, cystatin-C, creatinine or beta-2- microglobulin.
Researchers conducted multivariable linear and logistic regression models fit for each individual predictor based on a predictor cage equivalent to 1 interquartile range.
Regardless of how GFR was estimated, a lower eGFR correlated with reduced cortex volume, increased log-white matter hyperintensity volume and reduced white matter fractional anisotropy. Similarly, a higher log-UACR was linked with these outcomes, brain infarcts and micro-hemorrhages. Analyses revealed that brain reduction was comparable to regions susceptible to AD and LATE instead of the rest of the cortex.
Researchers noted that AD and LATE may not significantly contribute to neurodegeneration associated with CKD.
“Compared to previous studies, our analysis adds a more detailed breakdown of affected brain regions. The effect size for the association of lower eGFR levels and reduced brain volume was similar in direction and magnitude for brain regions usually susceptible to AD and LATE and other regions of the cortex. The generalized atrophy pattern, which we observed for both eGFR and UACR, was not selective for regions typically affected by AD and LATE,” Scheppach and colleagues wrote. They added, “Our analysis shows statistically significant associations of impaired kidney function with brain atrophy, microvascular brain damage and impaired white matter integrity. Hence, CKD appears to be related to various domains of macro- and microstructural brain damage suggestive of a multifactorial pathomechanism in the development of neurodegeneration and brain small vascular disease.”
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