ArticleKidney medicine2025
Deoxycholic Acid and Cognitive Impairment and Decline in the Chronic Renal Insufficiency Cohort (CRIC).
Article in Kidney medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Ureic clearance granule ameliorates chronic kidney disease by reshaping microbial dysbiosis via modulating bile acid metabolism.Chinese medicine · 2026Article
- Microbiota-derived metabolites and cognitive dysfunction in dialysis patients: mechanisms and targeted therapeutic strategies.Frontiers in microbiology · 2026Review
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Authors and funding
19 authors.
Funding
Abstract
Rationale & Objective: Cognitive impairment is common in chronic kidney disease (CKD). The secondary bile acid, deoxycholic acid (DCA), is associated with cognitive impairment and Alzheimer's dementia among older adults without CKD. Whether DCA is associated with cognitive impairment and decline in CKD is unknown. Study Design: Cross-sectional and longitudinal multivariable-adjusted regression analyses. Setting & Participants: 2,836 CRIC Study participants; 699 CRIC Cognitive (COG) Study participants. Exposure: Fasting serum DCA levels measured at visit 5 (ie, baseline). Outcomes: Modified Mini-Mental State Examination (3MS) in the main CRIC cohort and domain-specific cognitive tests in the CRIC COG cohort: Trail Making Test Parts A and B, Category Fluency, Buschke Selective Reminding, and Boston Naming. Cognitive impairment was defined as test score >1 standard deviation worse than the mean test score. Results: Mean age 59 ± 10 years, 45% female, and 39% Black. In the overall cohort, in cross-sectional analyses, there was no association between DCA and cognitive impairment by 3MS in after adjustment for demographics and clinical factors (prevalence ratio doubling DCA, 1.00; 95% CI, 0.95-1.06; n = 2,836). In longitudinal analyses, DCA was associated with decline (mean annual percent change in 3MS per doubling DCA, -0.13; 95% CI, -0.28 to -0.02) but not with incident impairment (n = 2,836; follow-up of 8.6 ± 3.9 years). Among CRIC COG Study participants, in cross-sectional analyses, DCA was associated with cognitive impairment based on Category Fluency (prevalence ratio per doubling DCA, 1.14; 95% CI, 1.02-1.27) but not with other specific-domain cognitive tests (n = 698-699). In CRIC COG longitudinal analyses, DCA was not associated with decline or incident cognitive impairment (n = 538-574). Limitations: No adjustment for inflammation, no stool DCA, 3MS may lack specificity. Conclusion: Among individuals with CKD stages 2-4, higher DCA levels were independently associated with prevalent cognitive impairment in Category Fluency. The association between DCA and progressive cognitive impairment assessed by 3MS was small and likely not clinically significant.
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